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mouse p75 ntr (Alomone Labs)

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Alomone Labs mouse p75 ntr

Characterization of ENCDC cultures. Flow cytometry of ENCDC cultures stained with antibodies against the immature neuronal marker, <t>p75</t> <t>NTR+</t> ‐FITC demonstrated 95.1% p75 NTR+ ‐positive, 97.3% viability in subculture 3, and 96.1% p75 NTR+ ‐positive, 98.2% viability in subculture 4 (a). Proportion of ENCDC cultures characterized for expression of p75NTR+, pH3, 5‐HT, nNOS, and TH. Scale bar = 20 µm (b). There was a significant increase in the proportion of serotonergic neurons and nitrergic neurons in subculture 5 (gray) compared to subculture 4 (black), but no significant difference in proliferating cells or dopaminergic neurons across the cultures. *p ≤ .05. Values are presented as mean ± SEM (c)

Mouse P75 Ntr, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 90/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse p75 ntr/product/Alomone Labs
Average 90 stars, based on 6 article reviews

mouse p75 ntr - by Bioz Stars, 2026-03

90/100 stars

Images

1) Product Images from "Influence of bacterial components on the developmental programming of enteric neurons"

Article Title: Influence of bacterial components on the developmental programming of enteric neurons

Journal: Physiological Reports

doi: 10.14814/phy2.14611

Characterization of ENCDC cultures. Flow cytometry of ENCDC cultures stained with antibodies against the immature neuronal marker, p75 NTR+ ‐FITC demonstrated 95.1% p75 NTR+ ‐positive, 97.3% viability in subculture 3, and 96.1% p75 NTR+ ‐positive, 98.2% viability in subculture 4 (a). Proportion of ENCDC cultures characterized for expression of p75NTR+, pH3, 5‐HT, nNOS, and TH. Scale bar = 20 µm (b). There was a significant increase in the proportion of serotonergic neurons and nitrergic neurons in subculture 5 (gray) compared to subculture 4 (black), but no significant difference in proliferating cells or dopaminergic neurons across the cultures. *p ≤ .05. Values are presented as mean ± SEM (c)

Figure Legend Snippet: Characterization of ENCDC cultures. Flow cytometry of ENCDC cultures stained with antibodies against the immature neuronal marker, p75 NTR+ ‐FITC demonstrated 95.1% p75 NTR+ ‐positive, 97.3% viability in subculture 3, and 96.1% p75 NTR+ ‐positive, 98.2% viability in subculture 4 (a). Proportion of ENCDC cultures characterized for expression of p75NTR+, pH3, 5‐HT, nNOS, and TH. Scale bar = 20 µm (b). There was a significant increase in the proportion of serotonergic neurons and nitrergic neurons in subculture 5 (gray) compared to subculture 4 (black), but no significant difference in proliferating cells or dopaminergic neurons across the cultures. *p ≤ .05. Values are presented as mean ± SEM (c)

Techniques Used: Flow Cytometry, Staining, Marker, Expressing

Image Search Results

MPCs expressing p75 NTR migrate into the laser-injured area of RPE-Choroid. p75 NTR co-localizes in F4/80 positive cells in RPE-Choroid. Tissue extracts and flat-mounted retinas were prepared and evaluated by Western blot and by IHC. ( A ) Representative Western blot of RPE-Choroid homogenates prepared from WT mice without CNV, or 4 days after laser injury. Tubulin was used as loading control. Bands were quantified by densitometric analysis, and p75 NTR /tubulin ratio is represented in the bar graph expressed as units relative to control. Bars denote the mean ± SD from triplicate experiments, n = 5 mice/group. The asterisks show statistical differences respect to control. * p < 0.05. ( B ) Representative Western blot of RPE-Choroid homogenates prepared from WT mice without CNV, or 7 days after laser injury. Tubulin was used as loading control. Bands were quantified by densitometric analysis, and p75 NTR /tubulin ratio is represented in the bar graph expressed as units relative to control. ns: non-significant. Bars denote the mean ± SD from triplicate experiments, n = at least 4 mice/group. ( C – E ) Representative confocal images of RPE-Choroid flat-mounts of WT mice 4 days after laser injury, showing immunofluorescence staining with: ( C ) F4/80 (green), p75 NTR (red) and cell nuclei (blue). Scale bar upper panel: 50 µm. Scale bar lower panel: 20 µm. ( D ) IBA-1 (green), p75 NTR (red) and cell nuclei (blue). Scale bar upper panel: 100 µm. Scale bar lower panel: 50 µm. ( E ) CX3CR1 (green), p75 NTR (red) and cell nuclei (blue). Scale bar upper panel: 100 µm. Scale bar lower panel: 25 µm. ( F , G ) Representative confocal images of RPE-Choroid flat-mounts of WT mice 7 days after laser injury, showing immunofluorescence staining with ( F ) Isolectin IB-4 (green), p75 NTR (red) and cell nuclei (blue). Scale bar: 50 µm. ( G ) NG-2 (green), p75 NTR (red) and cell nuclei (blue). Scale bar: 50 µm.

Journal: Cells

Article Title: Etiological Roles of p75 NTR in a Mouse Model of Wet Age-Related Macular Degeneration

doi: 10.3390/cells12020297

Figure Lengend Snippet: MPCs expressing p75 NTR migrate into the laser-injured area of RPE-Choroid. p75 NTR co-localizes in F4/80 positive cells in RPE-Choroid. Tissue extracts and flat-mounted retinas were prepared and evaluated by Western blot and by IHC. ( A ) Representative Western blot of RPE-Choroid homogenates prepared from WT mice without CNV, or 4 days after laser injury. Tubulin was used as loading control. Bands were quantified by densitometric analysis, and p75 NTR /tubulin ratio is represented in the bar graph expressed as units relative to control. Bars denote the mean ± SD from triplicate experiments, n = 5 mice/group. The asterisks show statistical differences respect to control. * p < 0.05. ( B ) Representative Western blot of RPE-Choroid homogenates prepared from WT mice without CNV, or 7 days after laser injury. Tubulin was used as loading control. Bands were quantified by densitometric analysis, and p75 NTR /tubulin ratio is represented in the bar graph expressed as units relative to control. ns: non-significant. Bars denote the mean ± SD from triplicate experiments, n = at least 4 mice/group. ( C – E ) Representative confocal images of RPE-Choroid flat-mounts of WT mice 4 days after laser injury, showing immunofluorescence staining with: ( C ) F4/80 (green), p75 NTR (red) and cell nuclei (blue). Scale bar upper panel: 50 µm. Scale bar lower panel: 20 µm. ( D ) IBA-1 (green), p75 NTR (red) and cell nuclei (blue). Scale bar upper panel: 100 µm. Scale bar lower panel: 50 µm. ( E ) CX3CR1 (green), p75 NTR (red) and cell nuclei (blue). Scale bar upper panel: 100 µm. Scale bar lower panel: 25 µm. ( F , G ) Representative confocal images of RPE-Choroid flat-mounts of WT mice 7 days after laser injury, showing immunofluorescence staining with ( F ) Isolectin IB-4 (green), p75 NTR (red) and cell nuclei (blue). Scale bar: 50 µm. ( G ) NG-2 (green), p75 NTR (red) and cell nuclei (blue). Scale bar: 50 µm.

Article Snippet: Afterwards, RPE-Choroids were incubated overnight with 0.01 μg/μL of Isolectin IB4 Alexa fluor-488 conjugate (GSA-IB4) from Molecular Probes, Inc. (Eugene, OR, USA), phalloidin-Alexa Fluor 647 (Thermo Fisher Scientific, A22287, Waltham, MA, USA), goat polyclonal anti-p75 NTR (1/500; R&D system), mouse anti f4/80 (1/50; Invitrogen, Waltham, MA, USA), rabbit anti CX3CR1 (1/100; Abcam, ab8021, Cambridge, UK), rabbit polyclonal anti-iba1 (1/200; Wako 019-19741), or rabbit polyclonal anti-NG-2 (1/100; AB5320, Millipore, Burlington, MA, USA).

Techniques: Expressing, Western Blot, Control, Immunofluorescence, Staining

Activated macroglial cells express p75 NTR after the laser around the injured area in the retina. p75 NTR protein co-localizes with GFAP-positive activated macroglia in CNV mice retinas, 7 days after laser. Tissue extracts and retina sections were prepared and evaluated by Western blot and by IHC. ( A ) Representative Western blot of total retinas homogenates prepared from WT mice without CNV, or 7 days after laser injury. (+) Correspond to a positive control (hippocampus E19 M2). Actin was used as loading control. Bands were quantified by densitometric analysis, and p75 NTR /actin ratio is represented in the bar graph expressed as units relative to control. Bars denote the mean ± SD from triplicate experiments, n = 6 mice/group. The asterisks show statistical differences respect to control. * p < 0.05. ( B ) Representative confocal images of WT CNV mice retinal cryosections, 7 days after laser. Upper panel: immunofluorescence staining of GFAP (green) and p75 NTR (red). Scale bar: 50 µm. * Indicates the injured area. Zoom scale bar: 25 µm. Cell nuclei counterstained with Hoechst are also shown (blue). Lower panel: immunofluorescence staining of β3 tubulin (green) and p75 NTR (red). Scale bar: 25 µm. Zoom scale bar: 10 µm. Abbreviations: GCL (ganglion cells layer), IPL (inner plexiform layer), INL (inner nuclear layer), OPL (outer plexiform layer), ONL (outer nuclear layer). ( C ) Representative confocal images of retinal flat-mount of WT CNV mice, 7 days after laser, showing immunofluorescence staining with NG-2 (green) and p75 NTR (red). Scale bar: 50 µm.

Journal: Cells

Article Title: Etiological Roles of p75 NTR in a Mouse Model of Wet Age-Related Macular Degeneration

doi: 10.3390/cells12020297

Figure Lengend Snippet: Activated macroglial cells express p75 NTR after the laser around the injured area in the retina. p75 NTR protein co-localizes with GFAP-positive activated macroglia in CNV mice retinas, 7 days after laser. Tissue extracts and retina sections were prepared and evaluated by Western blot and by IHC. ( A ) Representative Western blot of total retinas homogenates prepared from WT mice without CNV, or 7 days after laser injury. (+) Correspond to a positive control (hippocampus E19 M2). Actin was used as loading control. Bands were quantified by densitometric analysis, and p75 NTR /actin ratio is represented in the bar graph expressed as units relative to control. Bars denote the mean ± SD from triplicate experiments, n = 6 mice/group. The asterisks show statistical differences respect to control. * p < 0.05. ( B ) Representative confocal images of WT CNV mice retinal cryosections, 7 days after laser. Upper panel: immunofluorescence staining of GFAP (green) and p75 NTR (red). Scale bar: 50 µm. * Indicates the injured area. Zoom scale bar: 25 µm. Cell nuclei counterstained with Hoechst are also shown (blue). Lower panel: immunofluorescence staining of β3 tubulin (green) and p75 NTR (red). Scale bar: 25 µm. Zoom scale bar: 10 µm. Abbreviations: GCL (ganglion cells layer), IPL (inner plexiform layer), INL (inner nuclear layer), OPL (outer plexiform layer), ONL (outer nuclear layer). ( C ) Representative confocal images of retinal flat-mount of WT CNV mice, 7 days after laser, showing immunofluorescence staining with NG-2 (green) and p75 NTR (red). Scale bar: 50 µm.

Techniques: Western Blot, Positive Control, Control, Immunofluorescence, Staining

Reduced inflammatory phenotype in the RPE-Choroids and retinas of p75 NTR knockout mice, after laser injury. Mononuclear phagocytic cell recruitment is significantly reduced in retinas and RPE-Choroids of p75 NTR KO mice after CNV. ( A ) Representative flow cytometry pseudocolor plots from WT and p75 NTR KO mice without CNV, or 4 days after laser injury. Cells in the gate were quantified and the number of cells in the gate/total cells ratio is represented in the bar graph expressed as units relative to WT no laser control. Graphs denote the mean ± SD from triplicate experiments, n = 6 mice/group. The asterisks show statistical differences respect to control. * p < 0.05, ** p < 0.01, *** p < 0.001. ( B ) Representative confocal images of RPE-Choroid flat-mounts of WT and p75 NTR KO mice 4 days after laser, showing immunofluorescence staining with Isolectin IB-4 (grey) and F4/80 (green). Scale bar: 200 µm. F4/80 fluorescence intensity and area were quantified with ImageJ FIJI software Version 1.53t, and represented in the bar graph expressed as units relative to CNV WT control. Bars denote the mean ± SD from triplicate experiments, n = at least 5 mice/group. ns: non-significant.

Journal: Cells

Article Title: Etiological Roles of p75 NTR in a Mouse Model of Wet Age-Related Macular Degeneration

doi: 10.3390/cells12020297

Figure Lengend Snippet: Reduced inflammatory phenotype in the RPE-Choroids and retinas of p75 NTR knockout mice, after laser injury. Mononuclear phagocytic cell recruitment is significantly reduced in retinas and RPE-Choroids of p75 NTR KO mice after CNV. ( A ) Representative flow cytometry pseudocolor plots from WT and p75 NTR KO mice without CNV, or 4 days after laser injury. Cells in the gate were quantified and the number of cells in the gate/total cells ratio is represented in the bar graph expressed as units relative to WT no laser control. Graphs denote the mean ± SD from triplicate experiments, n = 6 mice/group. The asterisks show statistical differences respect to control. * p < 0.05, ** p < 0.01, *** p < 0.001. ( B ) Representative confocal images of RPE-Choroid flat-mounts of WT and p75 NTR KO mice 4 days after laser, showing immunofluorescence staining with Isolectin IB-4 (grey) and F4/80 (green). Scale bar: 200 µm. F4/80 fluorescence intensity and area were quantified with ImageJ FIJI software Version 1.53t, and represented in the bar graph expressed as units relative to CNV WT control. Bars denote the mean ± SD from triplicate experiments, n = at least 5 mice/group. ns: non-significant.

Techniques: Knock-Out, Flow Cytometry, Control, Immunofluorescence, Staining, Fluorescence, Software

Reduced neovascular phenotype in the choroid of p75 NTR knockout mice, after laser injury. The area and the perimeter of choroidal neovessels are significantly reduced in RPE-Choroid flat-mounts of p75 NTR KO mice. ( A ) Representative confocal images of RPE-Choroid flat-mounts of WT and p75 NTR KO mice 1 day after laser injury, showing immunofluorescence staining with Falloidin (green). The yellow outline represents the lesioned area estimated by F-actin negative staining. Scale bar: 15 µm. Cell nuclei counterstained with Hoechst are also shown (blue). The area and perimeter of the laser lesion were quantified with ImageJ FIJI software, and represented in the bar graph expressed as units relative to WT CNV control. Bars denote the mean ± SD from triplicate experiments, n = 4 mice/group. ns: non-significant. ( B ) Representative confocal images of RPE-Choroid flat-mounts of WT mice 7 days after laser injury, showing immunofluorescence staining with Isolectin IB-4 (green). The yellow outline represents the neovessels covered area. Scale bar: 200 µm. The area and the perimeter of the neovessels were quantified with ImageJ FIJI software, and represented in the bar graph expressed as units relative to CNV WT control. Bars denote the mean ± SD from triplicate experiments, n = at least 6 mice/group. The asterisks show statistical differences respect to control. * p < 0.05, ** p < 0.01, *** p < 0.001. ( C ) Representative Western blot of total retinal homogenates prepared from WT and p75 NTR KO mice without CNV, or 7 days after laser injury. Tubulin was used as loading control. Bands were quantified by densitometric analysis, and GFAP/tubulin ratio is represented in the bar graph expressed as units relative to control. Bars denote the mean ± SD from triplicate experiments, n = 3 mice/group. ( D ) Representative immunofluorescence analysis of GFAP (green) in retinal cryosections from WT and p75 NTR KO mice without injury or 7 days after laser injury. Scale bar: 50 µm. Cell nuclei counterstained with Hoechst are also shown (blue). Abbreviations: GCL (ganglion cells layer), IPL (inner plexiform layer), INL (inner nuclear layer), OPL (outer plexiform layer), ONL (outer nuclear layer). ( E ) Amplitudes and implicit times of a- and b-waves from scotopic electroretinograms recorded in WT and p75 NTR KO mice without injury or 7 days after laser injury. The data show averages of responses of both eyes. Graphs denote the mean ± SD from triplicate experiments, n = at least 6 mice/group. The symbol correspond: WT no laser (filled circle), WT CNV (filled square), p75 NTR KO no laser (filled triangle up), p75 NTR KO CNV (filled triangle down). The asterisks show statistical differences respect to control. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Cells

Article Title: Etiological Roles of p75 NTR in a Mouse Model of Wet Age-Related Macular Degeneration

doi: 10.3390/cells12020297

Figure Lengend Snippet: Reduced neovascular phenotype in the choroid of p75 NTR knockout mice, after laser injury. The area and the perimeter of choroidal neovessels are significantly reduced in RPE-Choroid flat-mounts of p75 NTR KO mice. ( A ) Representative confocal images of RPE-Choroid flat-mounts of WT and p75 NTR KO mice 1 day after laser injury, showing immunofluorescence staining with Falloidin (green). The yellow outline represents the lesioned area estimated by F-actin negative staining. Scale bar: 15 µm. Cell nuclei counterstained with Hoechst are also shown (blue). The area and perimeter of the laser lesion were quantified with ImageJ FIJI software, and represented in the bar graph expressed as units relative to WT CNV control. Bars denote the mean ± SD from triplicate experiments, n = 4 mice/group. ns: non-significant. ( B ) Representative confocal images of RPE-Choroid flat-mounts of WT mice 7 days after laser injury, showing immunofluorescence staining with Isolectin IB-4 (green). The yellow outline represents the neovessels covered area. Scale bar: 200 µm. The area and the perimeter of the neovessels were quantified with ImageJ FIJI software, and represented in the bar graph expressed as units relative to CNV WT control. Bars denote the mean ± SD from triplicate experiments, n = at least 6 mice/group. The asterisks show statistical differences respect to control. * p < 0.05, ** p < 0.01, *** p < 0.001. ( C ) Representative Western blot of total retinal homogenates prepared from WT and p75 NTR KO mice without CNV, or 7 days after laser injury. Tubulin was used as loading control. Bands were quantified by densitometric analysis, and GFAP/tubulin ratio is represented in the bar graph expressed as units relative to control. Bars denote the mean ± SD from triplicate experiments, n = 3 mice/group. ( D ) Representative immunofluorescence analysis of GFAP (green) in retinal cryosections from WT and p75 NTR KO mice without injury or 7 days after laser injury. Scale bar: 50 µm. Cell nuclei counterstained with Hoechst are also shown (blue). Abbreviations: GCL (ganglion cells layer), IPL (inner plexiform layer), INL (inner nuclear layer), OPL (outer plexiform layer), ONL (outer nuclear layer). ( E ) Amplitudes and implicit times of a- and b-waves from scotopic electroretinograms recorded in WT and p75 NTR KO mice without injury or 7 days after laser injury. The data show averages of responses of both eyes. Graphs denote the mean ± SD from triplicate experiments, n = at least 6 mice/group. The symbol correspond: WT no laser (filled circle), WT CNV (filled square), p75 NTR KO no laser (filled triangle up), p75 NTR KO CNV (filled triangle down). The asterisks show statistical differences respect to control. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Knock-Out, Immunofluorescence, Staining, Negative Staining, Software, Control, Western Blot

Reduced neovascular phenotype and improved retinal function in p75 NTR antagonist-treated wild type mice after laser injury. p75 NTR receptor antagonist reduced the area and perimeter of choroidal neovessels and improved retinal functionality in WT CNV mice. ( A ) Representative confocal images of RPE-Choroid flat-mounts of WT mice 7 days after laser, showing immunofluorescence staining with Isolectin IB-4 (grey). Scale bar: 100 µm. ( B ) The area and perimeter of neovessels were quantified with ImageJ FIJI software and represented in the bar graph expressed as units relative to WT CNV vehicle control. Bars denote the mean ± SD from triplicate experiments, n = 5 mice/group. ( C ) Amplitudes and implicit times of a- and b-waves from scotopic electroretinograms recorded 7 days after the laser in WT and WT CNV mice injected with THX-B or vehicle. The data show averages of responses of both. Graphs denote the mean ± SD from triplicate experiments, n = at least 6 mice/group. ( D ) Representative flow cytometry pseudocolor plots from WT CNV and no laser mice injected with THX-B or vehicle, 4 days after laser. Cells in the gate were quantified and the number of cells in the gate/total cells ratio is represented in the bar graph expressed as units relative to WT no laser vehicle control. Graphs denote the mean ± SD from triplicate experiments, n = 6 mice/group. The symbol correspond: No laser (white circle), CNV Vehicle (filled square), No laser THX B (filled triangle up), CNV THX B (filled triangle down). The asterisks show statistical differences respect to control. * p < 0.05, ** p < 0.01, *** p < 0.001. ( E ) Representative confocal images of RPE-Choroid flat-mounts of WT mice 4 days after laser, showing immunofluorescence staining with F4/80 (green). Scale bar: 200 µm. The area and the F4/80 fluorescence intensity were quantified with ImageJ FIJI software and represented in the bar graph expressed as units relative to WT CNV+ vehicle control. Bars denote the mean ± SD from triplicate experiments, n = 4 mice/group. ns: non-significant.

Journal: Cells

Article Title: Etiological Roles of p75 NTR in a Mouse Model of Wet Age-Related Macular Degeneration

doi: 10.3390/cells12020297

Figure Lengend Snippet: Reduced neovascular phenotype and improved retinal function in p75 NTR antagonist-treated wild type mice after laser injury. p75 NTR receptor antagonist reduced the area and perimeter of choroidal neovessels and improved retinal functionality in WT CNV mice. ( A ) Representative confocal images of RPE-Choroid flat-mounts of WT mice 7 days after laser, showing immunofluorescence staining with Isolectin IB-4 (grey). Scale bar: 100 µm. ( B ) The area and perimeter of neovessels were quantified with ImageJ FIJI software and represented in the bar graph expressed as units relative to WT CNV vehicle control. Bars denote the mean ± SD from triplicate experiments, n = 5 mice/group. ( C ) Amplitudes and implicit times of a- and b-waves from scotopic electroretinograms recorded 7 days after the laser in WT and WT CNV mice injected with THX-B or vehicle. The data show averages of responses of both. Graphs denote the mean ± SD from triplicate experiments, n = at least 6 mice/group. ( D ) Representative flow cytometry pseudocolor plots from WT CNV and no laser mice injected with THX-B or vehicle, 4 days after laser. Cells in the gate were quantified and the number of cells in the gate/total cells ratio is represented in the bar graph expressed as units relative to WT no laser vehicle control. Graphs denote the mean ± SD from triplicate experiments, n = 6 mice/group. The symbol correspond: No laser (white circle), CNV Vehicle (filled square), No laser THX B (filled triangle up), CNV THX B (filled triangle down). The asterisks show statistical differences respect to control. * p < 0.05, ** p < 0.01, *** p < 0.001. ( E ) Representative confocal images of RPE-Choroid flat-mounts of WT mice 4 days after laser, showing immunofluorescence staining with F4/80 (green). Scale bar: 200 µm. The area and the F4/80 fluorescence intensity were quantified with ImageJ FIJI software and represented in the bar graph expressed as units relative to WT CNV+ vehicle control. Bars denote the mean ± SD from triplicate experiments, n = 4 mice/group. ns: non-significant.

Techniques: Immunofluorescence, Staining, Software, Control, Injection, Flow Cytometry, Fluorescence

Journal: Physiological Reports

Article Title: Influence of bacterial components on the developmental programming of enteric neurons

doi: 10.14814/phy2.14611

Figure Lengend Snippet: Characterization of ENCDC cultures. Flow cytometry of ENCDC cultures stained with antibodies against the immature neuronal marker, p75 NTR+ ‐FITC demonstrated 95.1% p75 NTR+ ‐positive, 97.3% viability in subculture 3, and 96.1% p75 NTR+ ‐positive, 98.2% viability in subculture 4 (a). Proportion of ENCDC cultures characterized for expression of p75NTR+, pH3, 5‐HT, nNOS, and TH. Scale bar = 20 µm (b). There was a significant increase in the proportion of serotonergic neurons and nitrergic neurons in subculture 5 (gray) compared to subculture 4 (black), but no significant difference in proliferating cells or dopaminergic neurons across the cultures. *p ≤ .05. Values are presented as mean ± SEM (c)

Article Snippet: Single cells were incubated with primary antibody rabbit anti‐mouse p75 NTR+ for 1 hr (1:50, Alomone ANT‐007), and secondary antibody anti‐rabbit IgG microbeads for 15 min (150 µl per 10 7 cells; MACS Miltenyi Biotec 130‐048‐602).

Techniques: Flow Cytometry, Staining, Marker, Expressing

Images and quantitation of cholinotrophic basal forebrain neuron pathology within the nucleus basalis of Meynert in DSD+, DSD- and AMC cases (A–N) Photomicrographs show p75 NTR (brown, A-C), ChAT (purple, D-F) positive cells in AMC, DSD-, and DSD+ cases. Note the decrease in the number and intensity of both p75 NTR and ChAT labeled neurons in DSD- cases compared to an even greater reduction in DSD+ and globose shaped cells (black arrows) in DSD+ cases (C, F). Arrows in (A–F) mark cells shown at a higher magnification in the boxed areas located at the lower right corner of each panel. Dark brown AT8 (G, I) and TauC3 (H, J) bearing neurofibrillary tangles (NFTs) were observed only in the DSD- and DSD+ cases. Black arrows indicate globose shaped NFTs (G, H, and I) that are shown at a higher magnification in boxed areas adjacent to the lower magnification images. Note that not all neurons within the nbM (thin black arrows) contained tau pathology (G, H) in DSD- cases. Moreover, TauC3 staining revealed two NFT phenotypes that displayed either peripherally located or intense labeling that filled the entire structure (see boxed images adjacent to (H) and (J)). Scale bar in F = 50 μm and inset = 20 μm applies to panels A-E. Scale bar in J = 20 μm and inset = 20 μm applies to (G–J). Histograms show a significant reduction in both p75 NTR (K) and ChAT (L) positive cells in DSD+ compared to AMC. Although no significant were found in number of AT8 or TauC3 NFT positive cells (M), there was an increase in NTs in DSD+ compared to DSD- (N). ACM n = 5, DSD- n = 5, DSD+ n = 10. Data shown are presented as mean ± SEM. Statistical significance was determined using the Kruskal–Wallis’s test followed by Dunn’s test for comparisons across three clinical groups, and the Mann–Whitney test for comparisons between two groups (DSD- vs. DSD+). Significance levels (∗) were set at: ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Journal: iScience

Article Title: Cholinotrophic basal forebrain connectome dysfunction in Down syndrome with and without dementia

doi: 10.1016/j.isci.2025.113041

Figure Lengend Snippet: Images and quantitation of cholinotrophic basal forebrain neuron pathology within the nucleus basalis of Meynert in DSD+, DSD- and AMC cases (A–N) Photomicrographs show p75 NTR (brown, A-C), ChAT (purple, D-F) positive cells in AMC, DSD-, and DSD+ cases. Note the decrease in the number and intensity of both p75 NTR and ChAT labeled neurons in DSD- cases compared to an even greater reduction in DSD+ and globose shaped cells (black arrows) in DSD+ cases (C, F). Arrows in (A–F) mark cells shown at a higher magnification in the boxed areas located at the lower right corner of each panel. Dark brown AT8 (G, I) and TauC3 (H, J) bearing neurofibrillary tangles (NFTs) were observed only in the DSD- and DSD+ cases. Black arrows indicate globose shaped NFTs (G, H, and I) that are shown at a higher magnification in boxed areas adjacent to the lower magnification images. Note that not all neurons within the nbM (thin black arrows) contained tau pathology (G, H) in DSD- cases. Moreover, TauC3 staining revealed two NFT phenotypes that displayed either peripherally located or intense labeling that filled the entire structure (see boxed images adjacent to (H) and (J)). Scale bar in F = 50 μm and inset = 20 μm applies to panels A-E. Scale bar in J = 20 μm and inset = 20 μm applies to (G–J). Histograms show a significant reduction in both p75 NTR (K) and ChAT (L) positive cells in DSD+ compared to AMC. Although no significant were found in number of AT8 or TauC3 NFT positive cells (M), there was an increase in NTs in DSD+ compared to DSD- (N). ACM n = 5, DSD- n = 5, DSD+ n = 10. Data shown are presented as mean ± SEM. Statistical significance was determined using the Kruskal–Wallis’s test followed by Dunn’s test for comparisons across three clinical groups, and the Mann–Whitney test for comparisons between two groups (DSD- vs. DSD+). Significance levels (∗) were set at: ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: Antibodies were added to blocking buffer and membranes incubated overnight (4°C) in mouse anti-p75 NTR ([1:150], Santa Cruz Biotechnology Cat# sc-271708, RRID: AB_10714958 ), rabbit anti-ChAT ([1:500] (Proteintech Cat# 20747-1-AP, RRID: AB_10898169 ), rabbit anti-TrkA ([1:150], Fitzgerald Industries International Cat# 20R-TR013, RRID: AB_1289098 ) or rabbit anti-proNGF ([1:250], Alomone Labs Cat# ANT-005, RRID: AB_2040021 ), washed, incubated with horseradish peroxidase-conjugated with either a goat anti-mouse IgG (1:200) or goat anti-rabbit IgG (1:200) secondary antibody at RT, visualized by chemiluminescence (Kodak Image Station 440CF; Perkin-Elmer, Wellesley, MA), and quantified with Kodak 1.

Techniques: Quantitation Assay, Labeling, Staining, MANN-WHITNEY

Immunofluorescent images and quantification of p75 NTR neurons with and without AT8 and MAP2, as well as Thioflavin S single and AT8/Thioflavin S dual-labeled nbM cells in DSD+ and DSD-cases. (A–U) Immunofluorescent neurons labeled with p75 NTR (A, E, green), MAP2 (B, F, red), AT8 (C, G, Cyan), ThS (blue) (I, L) and merge images (D, H, K, N, R) in DSD- and DSD+ cases. In the DSD-cases there were greater p75 NTR cells AT8 negative neurons and p75 NTR MAP2 dual labeled neurons (A-D) compared to the DSD+ cases (E–H). Note that not all p75 NTR cells colocalize with AT8 or MAP2 in both DS groups (D, H). To determine the stage of a tangle tissue was stained for ThS, a marker of advanced pathology and the early stage AT8 phosphorylation antibody. Note that there are only a few ThS-labeled tangles that displayed AT8 in both DS groups (yellow arrows), compared to single ThS tangles, which were greater in DSD+ than in DSD- (white arrows) (I-L). Note that ThS positive NFTs that do not contain AT8 also do not colocalize with MAP2 (O-R). Scale bar in F = 25 μm applies to panels A-G, N = 25 μm applies to panels I-M and R = 10 μm and applies to O-Q. Graph showing a significant reduction in both p75 NTR AT8 immuno-negative, and p75 NTR MAP2 dual labeled neurons in DSD+ compared to DSD- (S). ThS-positive cells were greater (T), while the percentage of double-labeled cells with AT8 and ThS decreased (U) in DSD+ compared to individuals without dementia. DSD- n = 5, DSD+ n = 5. Data are presented as mean ± SEM. Statistical significance was determined using Mann–Whitney test for comparisons between DSD- and DSD+. Significance levels (∗) were set at: ∗ p < 0.05, ∗∗ p < 0.01.

Journal: iScience

Article Title: Cholinotrophic basal forebrain connectome dysfunction in Down syndrome with and without dementia

doi: 10.1016/j.isci.2025.113041

Figure Lengend Snippet: Immunofluorescent images and quantification of p75 NTR neurons with and without AT8 and MAP2, as well as Thioflavin S single and AT8/Thioflavin S dual-labeled nbM cells in DSD+ and DSD-cases. (A–U) Immunofluorescent neurons labeled with p75 NTR (A, E, green), MAP2 (B, F, red), AT8 (C, G, Cyan), ThS (blue) (I, L) and merge images (D, H, K, N, R) in DSD- and DSD+ cases. In the DSD-cases there were greater p75 NTR cells AT8 negative neurons and p75 NTR MAP2 dual labeled neurons (A-D) compared to the DSD+ cases (E–H). Note that not all p75 NTR cells colocalize with AT8 or MAP2 in both DS groups (D, H). To determine the stage of a tangle tissue was stained for ThS, a marker of advanced pathology and the early stage AT8 phosphorylation antibody. Note that there are only a few ThS-labeled tangles that displayed AT8 in both DS groups (yellow arrows), compared to single ThS tangles, which were greater in DSD+ than in DSD- (white arrows) (I-L). Note that ThS positive NFTs that do not contain AT8 also do not colocalize with MAP2 (O-R). Scale bar in F = 25 μm applies to panels A-G, N = 25 μm applies to panels I-M and R = 10 μm and applies to O-Q. Graph showing a significant reduction in both p75 NTR AT8 immuno-negative, and p75 NTR MAP2 dual labeled neurons in DSD+ compared to DSD- (S). ThS-positive cells were greater (T), while the percentage of double-labeled cells with AT8 and ThS decreased (U) in DSD+ compared to individuals without dementia. DSD- n = 5, DSD+ n = 5. Data are presented as mean ± SEM. Statistical significance was determined using Mann–Whitney test for comparisons between DSD- and DSD+. Significance levels (∗) were set at: ∗ p < 0.05, ∗∗ p < 0.01.

Techniques: Labeling, Staining, Marker, Phospho-proteomics, MANN-WHITNEY

FC cholinotrophic protein levels in AMC, DSD- and DSD+ (A–D) Representative immunoblots, and bar graphs show a significant upregulation of (A) proNGF and (B) p75 NTR , while (C) ChAT protein was downregulated between AMC and DSD+. (D) TrkA protein levels were stable across the groups analyzed. ACM n = 5, DSD- n = 5, DSD+ n = 13. Data are presented as mean ± SEM. Statistical significance was determined using the Kruskal–Wallis’s test followed by Dunn’s test for comparisons across three clinical groups. Significance levels (∗) were set at: ∗ p < 0.05.

Journal: iScience

Article Title: Cholinotrophic basal forebrain connectome dysfunction in Down syndrome with and without dementia

doi: 10.1016/j.isci.2025.113041

Figure Lengend Snippet: FC cholinotrophic protein levels in AMC, DSD- and DSD+ (A–D) Representative immunoblots, and bar graphs show a significant upregulation of (A) proNGF and (B) p75 NTR , while (C) ChAT protein was downregulated between AMC and DSD+. (D) TrkA protein levels were stable across the groups analyzed. ACM n = 5, DSD- n = 5, DSD+ n = 13. Data are presented as mean ± SEM. Statistical significance was determined using the Kruskal–Wallis’s test followed by Dunn’s test for comparisons across three clinical groups. Significance levels (∗) were set at: ∗ p < 0.05.

Techniques: Western Blot

Summary of changes in the cholinotrophic basal forebrain connectome in DS Diagrammatic sagittal view of the human brain (A) and a modified stacked bar graph (B) illustrating differences in the pathobiology of the cholinotrophic projection system between non-trisomy age-matched control (AMC), DS without dementia (DSD-) and DS with dementia (DSD+) individuals with DS. Frontal cortex protein levels for ChAT (pink), proNGF (green), p75 NTR (purple) and TrkA (light blue). Nucleus basalis NFTs of ThS (blue), AT8 (orange) and TauC3 (black) and counts of p75 NTR and ChAT (red) neurons. Created with BioRender.com .

Journal: iScience

Article Title: Cholinotrophic basal forebrain connectome dysfunction in Down syndrome with and without dementia

doi: 10.1016/j.isci.2025.113041

Figure Lengend Snippet: Summary of changes in the cholinotrophic basal forebrain connectome in DS Diagrammatic sagittal view of the human brain (A) and a modified stacked bar graph (B) illustrating differences in the pathobiology of the cholinotrophic projection system between non-trisomy age-matched control (AMC), DS without dementia (DSD-) and DS with dementia (DSD+) individuals with DS. Frontal cortex protein levels for ChAT (pink), proNGF (green), p75 NTR (purple) and TrkA (light blue). Nucleus basalis NFTs of ThS (blue), AT8 (orange) and TauC3 (black) and counts of p75 NTR and ChAT (red) neurons. Created with BioRender.com .

Techniques: Modification, Control

Analysis of CPF action on p-P38α ( A ), P75 NTR ( B ), and PAI-1 ( C ) levels. Results are shown as a percentage of control values. Results of protein content were normalized by total protein concentrations. *** p ≤ 0.001 compared to control. &&& p ≤ 0.001 compared to P38α -silenced cells exposed to CPF.

Journal: Foods

Article Title: Increased Levels of Phosphorylated-P38α Induce WNT/β-Catenin and NGF/P75NTR/TrkA Pathways Disruption and SN56 Cell Death following Single and Repeated Chlorpyrifos Treatment

doi: 10.3390/foods13152427

Figure Lengend Snippet: Analysis of CPF action on p-P38α ( A ), P75 NTR ( B ), and PAI-1 ( C ) levels. Results are shown as a percentage of control values. Results of protein content were normalized by total protein concentrations. *** p ≤ 0.001 compared to control. &&& p ≤ 0.001 compared to P38α -silenced cells exposed to CPF.

Article Snippet: SN56 cells were transfected using siRNA (Qiagen, Barcelona, Spain) homologous to mouse P75 NTR (GS18053), and P38α (GS26416) target genes following the HiPerfect Transfection reagent guideline.

Techniques: Control

Results from cell viability (MTT assay) ( A ) and apoptosis (caspase 3/7 activity assay) ( B ). Results were normalized by total protein concentrations. Results are shown as a percentage of control values. *** p ≤ 0.001 compared to control. ### p ≤ 0.001 compared to CPF treatment. &&& p ≤ 0.001 compared to P75 NTR -silenced cells treated with CPF. γγγ p ≤ 0.001 compared to rβ-Catenin and CPF treatment. τττ p ≤ 0.001 compared to P38α -silenced cells treated with CPF.

Journal: Foods

Article Title: Increased Levels of Phosphorylated-P38α Induce WNT/β-Catenin and NGF/P75NTR/TrkA Pathways Disruption and SN56 Cell Death following Single and Repeated Chlorpyrifos Treatment

doi: 10.3390/foods13152427

Figure Lengend Snippet: Results from cell viability (MTT assay) ( A ) and apoptosis (caspase 3/7 activity assay) ( B ). Results were normalized by total protein concentrations. Results are shown as a percentage of control values. *** p ≤ 0.001 compared to control. ### p ≤ 0.001 compared to CPF treatment. &&& p ≤ 0.001 compared to P75 NTR -silenced cells treated with CPF. γγγ p ≤ 0.001 compared to rβ-Catenin and CPF treatment. τττ p ≤ 0.001 compared to P38α -silenced cells treated with CPF.

Techniques: MTT Assay, Activity Assay, Control

| Construction of TEN in vitro and tracing of GFP-SKP-SCs in vivo . (a) Isolation and culture of SKPs from the back skin of 1 to 3-day-old newborn rat. HE staining and immunostainings of fibronectin, nestin, vimentin, and versican showed the location of SKPs around the dermal hair follicle area of the newborn rat. Phase contrast image showed the SKP spheres were generated from juvenile SKPs after 14 days of culture. (b) Characterizations by the immunostainings of nestin, sca-1, vimentin, fibronectin, and versican for SKPs and (c) the immunostainings of S100β, GFAP and p75 NTR for SKP-SCs. (d) The GFP-SKP-SCs cultured with chitosan/silk fibroin neural scaffolds in a perfusion bioreactor (termed the RCCMax system). (e) SEM images and immunofluorescence images showed the micromorphology of GFP-SKP-SCs cultured on silk fibroin filaments and chitosan conduit. (f) SCs markers (S100 β, GFAP and p75 NTR ) and ECM molecules (collagen I, collagen IV, fibronectin and laminin) were confirmed by immunostainings on the silk fibroin filaments 7 days post construction of TEN. (g) The GFP-SKP-SCs-containing, chitosan/SF-fabricated TEN was applied in repairing the 10 mm sciatic nerve defect in wild type rat. The grafting segment was obtained, sectioned longitudinally, and then subjected to GFP fluorescent monitoring under microscopic observation. A linear end-to-end arrangement of GFP-SKP-SCs was observed at the implantation site three weeks post-implantation of the TEN.

Journal: Bioactive Materials

Article Title: Skin derived precursors induced Schwann cells mediated tissue engineering-aided neuroregeneration across sciatic nerve defect

doi: 10.1016/j.bioactmat.2023.11.016

Figure Lengend Snippet: | Construction of TEN in vitro and tracing of GFP-SKP-SCs in vivo . (a) Isolation and culture of SKPs from the back skin of 1 to 3-day-old newborn rat. HE staining and immunostainings of fibronectin, nestin, vimentin, and versican showed the location of SKPs around the dermal hair follicle area of the newborn rat. Phase contrast image showed the SKP spheres were generated from juvenile SKPs after 14 days of culture. (b) Characterizations by the immunostainings of nestin, sca-1, vimentin, fibronectin, and versican for SKPs and (c) the immunostainings of S100β, GFAP and p75 NTR for SKP-SCs. (d) The GFP-SKP-SCs cultured with chitosan/silk fibroin neural scaffolds in a perfusion bioreactor (termed the RCCMax system). (e) SEM images and immunofluorescence images showed the micromorphology of GFP-SKP-SCs cultured on silk fibroin filaments and chitosan conduit. (f) SCs markers (S100 β, GFAP and p75 NTR ) and ECM molecules (collagen I, collagen IV, fibronectin and laminin) were confirmed by immunostainings on the silk fibroin filaments 7 days post construction of TEN. (g) The GFP-SKP-SCs-containing, chitosan/SF-fabricated TEN was applied in repairing the 10 mm sciatic nerve defect in wild type rat. The grafting segment was obtained, sectioned longitudinally, and then subjected to GFP fluorescent monitoring under microscopic observation. A linear end-to-end arrangement of GFP-SKP-SCs was observed at the implantation site three weeks post-implantation of the TEN.

Article Snippet: The following primary antibodies were used at the stated dilutions: mouse anti-nestin antibody (1:200, Millipore, Temecula, CA, USA), rabbit anti-Sca-1 (1:200, Merck Millipore, Darmstadt, Germany), rabbit anti-versican, fibronectin, vimentin, collagen I, collagen IV (1:200, Abcam, Cambridge, MA, USA), chicken anti-P0 (1:500, Aves Labs, Davis, CA, USA), mouse anti-S100β and anti-laminin (1:500, Sigma Aldrich, St Louis, MO, USA), rabbit anti-GFAP (1:500, Dako, Tokyo, Japan), mouse anti-p75 NTR (1:500, Chemicon, Temecula, CA, USA), mouse anti-NF200 (1:400, Abcam, Cambridge, MA,USA), and rabbit anti-MBP (1:500, Millipore, Billerica, MA, USA).

Techniques: In Vitro, In Vivo, Isolation, Staining, Generated, Cell Culture, Immunofluorescence

Analysis of spheres and their progeny. A : Immunocytochemical analysis of sphere colonies on day 7. Bright-field images and immunostaining of spheres for p63 (an epidermal stem/progenitor cell marker), p75 NTR (an epidermal basal progenitor cell marker), cytokeratins 3 and 12 (differentiated epithelial cell markers, nestin (a neural stem cell marker), microtubule-associated protein 2 (MAP2: a differentiated neuronal cell marker), and neuron-specific enolase (NSE: a differentiated neuronal cell marker). Each colony has been labeled by BrdU. As a control, IgG was used instead of the primary antibody. Scale bar=100 µm. B : Double immunocytochemical staining of a sphere colony. The spheres are double immunostained by nestin and cytokeratin 12 or by p63 and alpha smooth muscle actin (αSMA). Scale bar=100 µm. C : RT–PCR of corneal epithelial tissues, spheres, and their progeny. Genes for P63 , keratin 3, keratin 12, and nestin are present in corneal epithelial tissues, spheres, and their progeny derived from the limbal or central regions, but not in total RNA processed without reverse-transcription. D : Immunocytochemical analysis of differentiated cells obtained from spheres. Cells migrating out of the spheres express both cytokeratin 3 and cytokeratin 12 (differentiated epithelial cell markers). These cells are also positive for MAP2, and NSE. Scale bar=100 µm.

Journal: Molecular Vision

Article Title: Isolation of adult progenitor cells with neuronal potential from rabbit corneal epithelial cells in serum- and feeder layer-free culture conditions

doi:

Figure Lengend Snippet: Analysis of spheres and their progeny. A : Immunocytochemical analysis of sphere colonies on day 7. Bright-field images and immunostaining of spheres for p63 (an epidermal stem/progenitor cell marker), p75 NTR (an epidermal basal progenitor cell marker), cytokeratins 3 and 12 (differentiated epithelial cell markers, nestin (a neural stem cell marker), microtubule-associated protein 2 (MAP2: a differentiated neuronal cell marker), and neuron-specific enolase (NSE: a differentiated neuronal cell marker). Each colony has been labeled by BrdU. As a control, IgG was used instead of the primary antibody. Scale bar=100 µm. B : Double immunocytochemical staining of a sphere colony. The spheres are double immunostained by nestin and cytokeratin 12 or by p63 and alpha smooth muscle actin (αSMA). Scale bar=100 µm. C : RT–PCR of corneal epithelial tissues, spheres, and their progeny. Genes for P63 , keratin 3, keratin 12, and nestin are present in corneal epithelial tissues, spheres, and their progeny derived from the limbal or central regions, but not in total RNA processed without reverse-transcription. D : Immunocytochemical analysis of differentiated cells obtained from spheres. Cells migrating out of the spheres express both cytokeratin 3 and cytokeratin 12 (differentiated epithelial cell markers). These cells are also positive for MAP2, and NSE. Scale bar=100 µm.

Article Snippet: The following antibodies were used: mouse anti-cytokeratin 3 monoclonal antibody (1:2,000; AE-5; Progen Biotechnik GMBH, Heidelberg, Germany), goat anti-cytokeratin 12 polyclonal antibody (1:2,000; L-20; Santa Cruz Biotech, Santa Cruz, CA), mouse monoclonal anti-p63 antibody (1:400; Imgenex, San Diego, CA), mouse monoclonal anti-nestin antibody (1:400; BD Biosciences), mouse monoclonal anti-nerve growth factor (NGF) receptor p75 NTR antibody (1:400; DAKO, Kyoto, Japan), Cy3-conjugated mouse anti-α-smooth muscle actin (SMA) mAb (1:400; Sigma-Aldrich), mouse monoclonal anti-nestin antibody (1:400; BD Biosciences), mouse monoclonal anti- microtubule-associated protein 2 antibody (MAP2, 1:400; Chemicon, Temecula, CA), mouse monoclonal anti- neuron specific enolase antibody (NSE, 1:400; DAKO), and mouse monoclonal anti-BrdU/fluorescein antibody (1:100; Roche Diagnostics, Basel, Switzerland).

Techniques: Immunostaining, Marker, Labeling, Staining, Reverse Transcription Polymerase Chain Reaction, Derivative Assay

Parallel sections from normal esophageal epithelial and ESCC specimen . (A) In NEE, p75 NTR was located mainly in the basal layer; in WDC, p75 NTR positive staining was apparent in the first one to two layers from the infiltrative margin, areas exhibiting stratified squamous pearl formation were negative for p75 NTR ; in MDC, p75 NTR was expressed in wider range from the margin of the tumors; p75 NTR was diffusely distributed in PDC.(B) In NEE, basal cells coexpressed p75 NTR and p63, and very few p75 NTR+ cells expressed ki-67; in WDC and MDC, p75 NTR+ cells were at some distance surrounding involucrin + cells where most of the cells were coexpressed p63, and a small proportion of p75 NTR+ cells expressed ki-67; in PDC, few cells were positive for involucrin, more cells contained both p63 and p75 NTR , and their distribution was chaotic, a large number of p75 NTR+ cells stained brightly for ki-67. (Bars = 200 μm)

Journal: BMC Cancer

Article Title: Self-renewal and chemotherapy resistance of p75 NTR positive cells in esophageal squamous cell carcinomas

doi: 10.1186/1471-2407-9-9

Figure Lengend Snippet: Parallel sections from normal esophageal epithelial and ESCC specimen . (A) In NEE, p75 NTR was located mainly in the basal layer; in WDC, p75 NTR positive staining was apparent in the first one to two layers from the infiltrative margin, areas exhibiting stratified squamous pearl formation were negative for p75 NTR ; in MDC, p75 NTR was expressed in wider range from the margin of the tumors; p75 NTR was diffusely distributed in PDC.(B) In NEE, basal cells coexpressed p75 NTR and p63, and very few p75 NTR+ cells expressed ki-67; in WDC and MDC, p75 NTR+ cells were at some distance surrounding involucrin + cells where most of the cells were coexpressed p63, and a small proportion of p75 NTR+ cells expressed ki-67; in PDC, few cells were positive for involucrin, more cells contained both p63 and p75 NTR , and their distribution was chaotic, a large number of p75 NTR+ cells stained brightly for ki-67. (Bars = 200 μm)

Article Snippet: Primary antibodies were: mouse anti human p75 NTR , involucrin, β1-integrin (Santa cruz Corporation, USA) and cytokeratin 13 (Santa cruz Corporation, USA).

Techniques: Staining

Relationship between p75 NTR expression and clinicopathologic characteristics

Journal: BMC Cancer

Article Title: Self-renewal and chemotherapy resistance of p75 NTR positive cells in esophageal squamous cell carcinomas

doi: 10.1186/1471-2407-9-9

Figure Lengend Snippet: Relationship between p75 NTR expression and clinicopathologic characteristics

Article Snippet: Primary antibodies were: mouse anti human p75 NTR , involucrin, β1-integrin (Santa cruz Corporation, USA) and cytokeratin 13 (Santa cruz Corporation, USA).

Techniques: Expressing

p75 NTR expression in ESCC cell line . p75 NTR+ cells made up 2.5% in Eca109 (A), 1.6% in SHEC-1 (B), 1.9% in SHEC-4 (C) and 3.7% (D) in SHEC-5. Cells derived from p75 NTR+ cells contained both p75 NTR+ and p75 NTR- cells, whereas those from p75 NTR- cells generated only p75 NTR- cells. In p75 NTR+ subpopulation, the percentage of p75 NTR+ cells declined time-dependently. In addition, p75 NTR+ cells could be serial passaged and generated p75 NTR+ β1-integrin - , p75 NTR- β1-integrin - and p75 NTR- β1-integrin + progenies (E), whereas p75 NTR- cells generated only p75 NTR- cells in 5th passage (F).

Journal: BMC Cancer

Article Title: Self-renewal and chemotherapy resistance of p75 NTR positive cells in esophageal squamous cell carcinomas

doi: 10.1186/1471-2407-9-9

Figure Lengend Snippet: p75 NTR expression in ESCC cell line . p75 NTR+ cells made up 2.5% in Eca109 (A), 1.6% in SHEC-1 (B), 1.9% in SHEC-4 (C) and 3.7% (D) in SHEC-5. Cells derived from p75 NTR+ cells contained both p75 NTR+ and p75 NTR- cells, whereas those from p75 NTR- cells generated only p75 NTR- cells. In p75 NTR+ subpopulation, the percentage of p75 NTR+ cells declined time-dependently. In addition, p75 NTR+ cells could be serial passaged and generated p75 NTR+ β1-integrin - , p75 NTR- β1-integrin - and p75 NTR- β1-integrin + progenies (E), whereas p75 NTR- cells generated only p75 NTR- cells in 5th passage (F).

Article Snippet: Primary antibodies were: mouse anti human p75 NTR , involucrin, β1-integrin (Santa cruz Corporation, USA) and cytokeratin 13 (Santa cruz Corporation, USA).

Techniques: Expressing, Derivative Assay, Generated

Different gene mRNA expression in p75 NTR+ and p75 NTR- subpopulation . mRNA expression level was measured by real-time qPCR. p63 (A) and Bmi-1 (B) were more intensely expressed in p75 NTR+ cells compared with p75 NTR- cells. Conversely, CTR1 (C), involucrin (D), cytokeratin 13 (E), β1-integrin (F) and β4-integrin (G) expression were lower.

Journal: BMC Cancer

Article Title: Self-renewal and chemotherapy resistance of p75 NTR positive cells in esophageal squamous cell carcinomas

doi: 10.1186/1471-2407-9-9

Figure Lengend Snippet: Different gene mRNA expression in p75 NTR+ and p75 NTR- subpopulation . mRNA expression level was measured by real-time qPCR. p63 (A) and Bmi-1 (B) were more intensely expressed in p75 NTR+ cells compared with p75 NTR- cells. Conversely, CTR1 (C), involucrin (D), cytokeratin 13 (E), β1-integrin (F) and β4-integrin (G) expression were lower.

Article Snippet: Primary antibodies were: mouse anti human p75 NTR , involucrin, β1-integrin (Santa cruz Corporation, USA) and cytokeratin 13 (Santa cruz Corporation, USA).

Techniques: Expressing

Sphere formation in serum-free medium . Tumor Cells formed nonadherent spheres in serum-free medium. The percentage of p75 NTR+ cells increased to 68.3% in Eca109, 62.7% in SHEC-1, 58.5% in SHEC-4 and 74.2% in SHEC-5 (A). Single p75 NTR+ cell could proliferate in serum-free culture and formed nonadherent cells sphere (B), contained both p75 NTR+ and p75 NTR- cells (C); p75 NTR+ cells obtained from the spheres did not expressed differentiated markers involucrin (D) and cytokeratin 13 (E). Floating p75 NTR+ cells could adhere and expressed involucrin (F) and cytokeratin 13 (G) in DMEM containing 10% fetal bovine serum. In addition, p75 NTR+ cells could be expanded as floating cell spheres for more than 30 passages, and the percentage of p75 NTR+ cells from passage 10, passage 20 and passage 30 was 66.4%, 56.3% and 59.2%, respectively (H). B and H bars = 100 μm. (F and G, bars = 50 μm)

Journal: BMC Cancer

Article Title: Self-renewal and chemotherapy resistance of p75 NTR positive cells in esophageal squamous cell carcinomas

doi: 10.1186/1471-2407-9-9

Figure Lengend Snippet: Sphere formation in serum-free medium . Tumor Cells formed nonadherent spheres in serum-free medium. The percentage of p75 NTR+ cells increased to 68.3% in Eca109, 62.7% in SHEC-1, 58.5% in SHEC-4 and 74.2% in SHEC-5 (A). Single p75 NTR+ cell could proliferate in serum-free culture and formed nonadherent cells sphere (B), contained both p75 NTR+ and p75 NTR- cells (C); p75 NTR+ cells obtained from the spheres did not expressed differentiated markers involucrin (D) and cytokeratin 13 (E). Floating p75 NTR+ cells could adhere and expressed involucrin (F) and cytokeratin 13 (G) in DMEM containing 10% fetal bovine serum. In addition, p75 NTR+ cells could be expanded as floating cell spheres for more than 30 passages, and the percentage of p75 NTR+ cells from passage 10, passage 20 and passage 30 was 66.4%, 56.3% and 59.2%, respectively (H). B and H bars = 100 μm. (F and G, bars = 50 μm)

Article Snippet: Primary antibodies were: mouse anti human p75 NTR , involucrin, β1-integrin (Santa cruz Corporation, USA) and cytokeratin 13 (Santa cruz Corporation, USA).

Techniques:

$DDP resistance of p75 NTR+ cells . Treated with 0.5 and 1 μg/ml DDP for 4 days, the number of viable cells in p75 NTR+ subpopulation was significant higher than that in p75 NTR- subpopulation. (B) Enrichment assay showed that the fraction of eGFP-carrying cells derived from p75 NTR+ cells increased from 9.4% to 48.1% and 86.2%, respectively. (C) Copper accumulation was less in the p75 NTR+ cells than in the p75 NTR- cells at each time point. (B, bars = 100 μm)$

Journal: BMC Cancer

Article Title: Self-renewal and chemotherapy resistance of p75 NTR positive cells in esophageal squamous cell carcinomas

doi: 10.1186/1471-2407-9-9

Figure Lengend Snippet: DDP resistance of p75 NTR+ cells . Treated with 0.5 and 1 μg/ml DDP for 4 days, the number of viable cells in p75 NTR+ subpopulation was significant higher than that in p75 NTR- subpopulation. (B) Enrichment assay showed that the fraction of eGFP-carrying cells derived from p75 NTR+ cells increased from 9.4% to 48.1% and 86.2%, respectively. (C) Copper accumulation was less in the p75 NTR+ cells than in the p75 NTR- cells at each time point. (B, bars = 100 μm)

Article Snippet: Primary antibodies were: mouse anti human p75 NTR , involucrin, β1-integrin (Santa cruz Corporation, USA) and cytokeratin 13 (Santa cruz Corporation, USA).

Techniques: Derivative Assay

Tumorigenicity of p75 NTR+ ESCC in NOD/SCID mice xenograft

Journal: BMC Cancer

Article Title: Self-renewal and chemotherapy resistance of p75 NTR positive cells in esophageal squamous cell carcinomas

doi: 10.1186/1471-2407-9-9

Figure Lengend Snippet: Tumorigenicity of p75 NTR+ ESCC in NOD/SCID mice xenograft

Article Snippet: Primary antibodies were: mouse anti human p75 NTR , involucrin, β1-integrin (Santa cruz Corporation, USA) and cytokeratin 13 (Santa cruz Corporation, USA).

Techniques: Injection

( A ) Schematic indicating the results of high-throughput cell-cell screening of B7-1 and p75 NTR against 395 members of the human Ig and TNFR superfamilies. B7-1–expressing cells bound to cells expressing CD28, CTLA-4, and p75 NTR , but not cells expressing PD-L1. p75 NTR –expressing cells bound to cells expressing B7-1 and PTPRF. ( B ) Representative flow plots demonstrating that hB7-1–mCherry cells and PTPRF-mCherry cells bind to cells expressing p75 NTR -GFP cells, but not GFP control cells. ( C ) Binding between B7-1 and p75 NTR was validated by recombinant protein titrations of p75 NTR -mIgG2A and CTLA-4–mIgG2A onto streptavidin beads coated with B7-1–hIgG1 biotin. Binding was detected using an anti-mIgG2A antibody, flow cytometry and binding curves were generated, and B max , EC 50 , and Hill coefficient (coeff.) were calculated using the equation Y = B max × X h /( Kd h + X h ). n = 2–3. Error bars represent SEM. ( D ) Cells expressing B7-1–mCherry from various mammalian species were screened against human p75 NTR -GFP–expressing cells (top left, n = 2–4), mouse p75 NTR -GFP–expressing cells (top right, n = 2–3), rat p75 NTR -GFP–expressing cells (bottom left n = 2–3), or cells expressing only GFP (bottom right, n = 3), indicating that B7-1:p75 NTR interactions are conserved in primates, but not mice. **** P < 0.0001, 1-way ANOVA with multiple comparisons. Each assay represents the indicated number of independent experiments, which each include a single replicate. For mouse B7-1, rat B7-1, and mCherry cells alone, only 2 independent experiments were conducted, each with 2 biological replicates.

Journal: The Journal of Clinical Investigation

Article Title: Human immunomodulatory ligand B7-1 mediates synaptic remodeling via the p75 neurotrophin receptor

doi: 10.1172/JCI157002

Figure Lengend Snippet: ( A ) Schematic indicating the results of high-throughput cell-cell screening of B7-1 and p75 NTR against 395 members of the human Ig and TNFR superfamilies. B7-1–expressing cells bound to cells expressing CD28, CTLA-4, and p75 NTR , but not cells expressing PD-L1. p75 NTR –expressing cells bound to cells expressing B7-1 and PTPRF. ( B ) Representative flow plots demonstrating that hB7-1–mCherry cells and PTPRF-mCherry cells bind to cells expressing p75 NTR -GFP cells, but not GFP control cells. ( C ) Binding between B7-1 and p75 NTR was validated by recombinant protein titrations of p75 NTR -mIgG2A and CTLA-4–mIgG2A onto streptavidin beads coated with B7-1–hIgG1 biotin. Binding was detected using an anti-mIgG2A antibody, flow cytometry and binding curves were generated, and B max , EC 50 , and Hill coefficient (coeff.) were calculated using the equation Y = B max × X h /( Kd h + X h ). n = 2–3. Error bars represent SEM. ( D ) Cells expressing B7-1–mCherry from various mammalian species were screened against human p75 NTR -GFP–expressing cells (top left, n = 2–4), mouse p75 NTR -GFP–expressing cells (top right, n = 2–3), rat p75 NTR -GFP–expressing cells (bottom left n = 2–3), or cells expressing only GFP (bottom right, n = 3), indicating that B7-1:p75 NTR interactions are conserved in primates, but not mice. **** P < 0.0001, 1-way ANOVA with multiple comparisons. Each assay represents the indicated number of independent experiments, which each include a single replicate. For mouse B7-1, rat B7-1, and mCherry cells alone, only 2 independent experiments were conducted, each with 2 biological replicates.

Article Snippet: Primary antibodies were anti-PSD95 (Abcam; catalog ab2723), anti-MAP2 (Abcam; catalog ab92434), anti-bassoon (Enzo, ADI-VAM-PS003-D clone, catalog SAP7F407), anti-GluR1 (Invitrogen, catalog PA1-46151), and anti-p75 NTR (R&D Systems; catalog AF1157).

Techniques: High Throughput Screening Assay, Expressing, Control, Binding Assay, Recombinant, Flow Cytometry, Generated

( A ) hB7-1 residues that when mutated showed more than 25% losses in binding to CD28 (blue) or both CD28 and CTLA-4 (green) mapped onto crystal structure of hB7-1 (PDB: 1I8L) ( B ) hB7-1 residues that when mutated showed more than 25% losses in binding to p75 NTR (red) mapped onto crystal structure of hB7-1 (PDB: 1I8L). ( C ) Same residues as in B , except with monomer of CTLA-4 shown. ( D ) CD28-hIgG1 competes for binding to B7-1 with p75 NTR . n = 6. ( E ) CTLA-4–mIgG2A competes for binding to B7-1 with p75 NTR . n = 3. Each assay represents the indicated number of independent experiments, which each include a single replicate. Error bars represent SEM.

Journal: The Journal of Clinical Investigation

Article Title: Human immunomodulatory ligand B7-1 mediates synaptic remodeling via the p75 neurotrophin receptor

doi: 10.1172/JCI157002

Figure Lengend Snippet: ( A ) hB7-1 residues that when mutated showed more than 25% losses in binding to CD28 (blue) or both CD28 and CTLA-4 (green) mapped onto crystal structure of hB7-1 (PDB: 1I8L) ( B ) hB7-1 residues that when mutated showed more than 25% losses in binding to p75 NTR (red) mapped onto crystal structure of hB7-1 (PDB: 1I8L). ( C ) Same residues as in B , except with monomer of CTLA-4 shown. ( D ) CD28-hIgG1 competes for binding to B7-1 with p75 NTR . n = 6. ( E ) CTLA-4–mIgG2A competes for binding to B7-1 with p75 NTR . n = 3. Each assay represents the indicated number of independent experiments, which each include a single replicate. Error bars represent SEM.

Techniques: Binding Assay

( A ) p75 NTR residues identified as important for hB7-1 binding mapped onto crystal structure of rat p75 NTR bound to NT3 (PDB: 3BUK) affect binding to B7-1 (red), make contacts with NT3 and also affect binding to B7-1 (brown), and make H bond contacts with NT3 (blue). ( B ) The hB7-1–binding site modeled onto the dimeric structure of p75 NTR bound to an NT3 dimer (PDB: 3BUK). ( C ) Ligand-competition experiments showing that NGF and hB7-1 compete for binding to p75 NTR at high concentrations. n = 3. ( D ) Cells expressing p75 NTR -F136K and F136H demonstrate binding to B7-1N82E–expressing cells as well as WT B7-1–expressing cells. **** P < 0.0001, 1-way ANOVA with multiple comparisons. n = 4. ( E ) Crystal structures of hB7-1 and p75 NTR indicating proposed interaction between p75 NTR -F136 and B7-1–N82. Each assay represents the indicated number of independent experiments, which each include a single replicate. Error bars represent SEM.

Journal: The Journal of Clinical Investigation

Article Title: Human immunomodulatory ligand B7-1 mediates synaptic remodeling via the p75 neurotrophin receptor

doi: 10.1172/JCI157002

Figure Lengend Snippet: ( A ) p75 NTR residues identified as important for hB7-1 binding mapped onto crystal structure of rat p75 NTR bound to NT3 (PDB: 3BUK) affect binding to B7-1 (red), make contacts with NT3 and also affect binding to B7-1 (brown), and make H bond contacts with NT3 (blue). ( B ) The hB7-1–binding site modeled onto the dimeric structure of p75 NTR bound to an NT3 dimer (PDB: 3BUK). ( C ) Ligand-competition experiments showing that NGF and hB7-1 compete for binding to p75 NTR at high concentrations. n = 3. ( D ) Cells expressing p75 NTR -F136K and F136H demonstrate binding to B7-1N82E–expressing cells as well as WT B7-1–expressing cells. **** P < 0.0001, 1-way ANOVA with multiple comparisons. n = 4. ( E ) Crystal structures of hB7-1 and p75 NTR indicating proposed interaction between p75 NTR -F136 and B7-1–N82. Each assay represents the indicated number of independent experiments, which each include a single replicate. Error bars represent SEM.

Techniques: Binding Assay, Expressing

( A ) Representative IF images of WT hippocampal neurons treated for 2 hours with proNGF (10 nM), hB7-1–Fc (750 nM), or hB7-2–Fc (750 nM) and stained for actin, PSD95, and MAP2. ( B ) Quantification of PSD95 puncta density with indicated treatments. Recombinant hB7-1–Fc but not hB7-2–Fc induced a decrease in PSD95 density in cultured neurons, similarly to proNGF treatment. ( C ) Representative IF images of p75 –/– hippocampal neurons treated with proNGF (10 nM), hB7-1–Fc (750 nM), or hB7-2–Fc (750 nM) and stained for actin, PSD95, and MAP2. ( D ) Quantification of PSD95 puncta density with indicated treatment. Recombinant hB7-1–Fc failed to induce a decrease in PSD95 density in cultured neurons. ( E ) Representative IF images of WT hippocampal neurons treated with hB7-1–Fc (750 nM) or hB7-2–Fc (750 nM) and stained for actin, GluR1, bassoon, and MAP2. ( F ) Quantification of bassoon puncta density with indicated treatment. ( G ) Quantification of GluR1 puncta density with indicated treatment. ** P < 0.01, 1-way ANOVA with Dunnett’s multiple-comparisons test. n = 3 independent experiments. Experiments under each condition were performed in triplicate, and 13 to 15 dendritic segments were analyzed per condition. Scale bar: 20 μm. Error bars represent SEM. See also .

Journal: The Journal of Clinical Investigation

Article Title: Human immunomodulatory ligand B7-1 mediates synaptic remodeling via the p75 neurotrophin receptor

doi: 10.1172/JCI157002

Figure Lengend Snippet: ( A ) Representative IF images of WT hippocampal neurons treated for 2 hours with proNGF (10 nM), hB7-1–Fc (750 nM), or hB7-2–Fc (750 nM) and stained for actin, PSD95, and MAP2. ( B ) Quantification of PSD95 puncta density with indicated treatments. Recombinant hB7-1–Fc but not hB7-2–Fc induced a decrease in PSD95 density in cultured neurons, similarly to proNGF treatment. ( C ) Representative IF images of p75 –/– hippocampal neurons treated with proNGF (10 nM), hB7-1–Fc (750 nM), or hB7-2–Fc (750 nM) and stained for actin, PSD95, and MAP2. ( D ) Quantification of PSD95 puncta density with indicated treatment. Recombinant hB7-1–Fc failed to induce a decrease in PSD95 density in cultured neurons. ( E ) Representative IF images of WT hippocampal neurons treated with hB7-1–Fc (750 nM) or hB7-2–Fc (750 nM) and stained for actin, GluR1, bassoon, and MAP2. ( F ) Quantification of bassoon puncta density with indicated treatment. ( G ) Quantification of GluR1 puncta density with indicated treatment. ** P < 0.01, 1-way ANOVA with Dunnett’s multiple-comparisons test. n = 3 independent experiments. Experiments under each condition were performed in triplicate, and 13 to 15 dendritic segments were analyzed per condition. Scale bar: 20 μm. Error bars represent SEM. See also .

Techniques: Staining, Recombinant, Cell Culture

( A ) Representative IF images of WT hippocampal neurons cocultured with HEK293–hB7-1, HEK293–hB7-2, or HEK293–hB7–1N82E treated with or without 375 nM abatacept. Differences in ( B ) MAP2 morphology in dendrites in direct contact with HEK-hB7 cell lines were quantified. Treatment with 375 nM abatacept could prevent the MAP2-positive process degeneration induced by the HEK293–B7-1 cell line. *** P < 0.001, 2-way ANOVA. n = 3 independent experiments in which 12 to 14 individual neurons were analyzed per treatment per experiment. Scale bar: 20 μm. ( C ) Representative IF images of p75 –/– hippocampal neurons cocultured with HEK293–B7-1, HEK293–B7-2, or HEK293–B7-1N82E treated with or without 375 nM abatacept. ( D ) No differences in MAP2 morphology in dendrites in direct contact with HEK-B7 cell lines (HEK293–B7-1, HEK293–B7-2, or HEK293–B7-1N82E treated with or without 375 nM abatacept) were found. P = 0.1860, 2-way ANOVA. n = 3 independent experiments. P < 0.01, 2-way ANOVA with multiple comparisons (WT coculture). Scale bar: 20 μm. See also . n = 3 independent experiments in which 12 to 14 individual neurons were analyzed per treatment per experiment. Error bars represent SEM.

Journal: The Journal of Clinical Investigation

Article Title: Human immunomodulatory ligand B7-1 mediates synaptic remodeling via the p75 neurotrophin receptor

doi: 10.1172/JCI157002

Figure Lengend Snippet: ( A ) Representative IF images of WT hippocampal neurons cocultured with HEK293–hB7-1, HEK293–hB7-2, or HEK293–hB7–1N82E treated with or without 375 nM abatacept. Differences in ( B ) MAP2 morphology in dendrites in direct contact with HEK-hB7 cell lines were quantified. Treatment with 375 nM abatacept could prevent the MAP2-positive process degeneration induced by the HEK293–B7-1 cell line. *** P < 0.001, 2-way ANOVA. n = 3 independent experiments in which 12 to 14 individual neurons were analyzed per treatment per experiment. Scale bar: 20 μm. ( C ) Representative IF images of p75 –/– hippocampal neurons cocultured with HEK293–B7-1, HEK293–B7-2, or HEK293–B7-1N82E treated with or without 375 nM abatacept. ( D ) No differences in MAP2 morphology in dendrites in direct contact with HEK-B7 cell lines (HEK293–B7-1, HEK293–B7-2, or HEK293–B7-1N82E treated with or without 375 nM abatacept) were found. P = 0.1860, 2-way ANOVA. n = 3 independent experiments. P < 0.01, 2-way ANOVA with multiple comparisons (WT coculture). Scale bar: 20 μm. See also . n = 3 independent experiments in which 12 to 14 individual neurons were analyzed per treatment per experiment. Error bars represent SEM.

Techniques:

( A ) Golgi-stained WT pyramidal neurons 3 hours after in vivo injection of hB7-1–Fc (100 ng), hB7-2–Fc (100 ng), or saline into the dSubiculum area of the hippocampal formation at P75. ( B ) There was a significant reduction in total spine density after 3 hours of hB7-1, compared with saline and the hB7-2 group. n = 4 mice/condition. ( C ) Golgi-stained p75 –/– pyramidal neurons 3 hours after in vivo injection of hB7-1–Fc (100 ng), hB7-2–Fc (100 ng), or saline into the dSubiculum area of the hippocampal formation at P75. n = 4 mice/condition ( D ) There were no significant changes in total spine density after 3 hours for the hB7-1 or hB7-2 group compared with the saline group. n = 4 mice/condition. ( E ) Golgi-stained WT pyramidal neurons 3 hours after in vivo injection of hB7-1–Fc (200 ng), hB7-2–Fc (200 ng), or saline into the dSubiculum area of the hippocampal formation at P75. ( F ) There was a significant reduction in total spine density after 3 hours of hB7-1, compared with the saline and hB7-2 groups. n = 4 mice/condition. ( G ) Golgi-stained WT pyramidal neurons 24 hours after in vivo injection of hB7-1–Fc (200 ng), hB7-2–Fc (200 ng), or saline into the dSubiculum area of the hippocampal formation at P75. ( H ) There was a significant reduction in total spine density after 24 hours of hB7-1, compared with the saline and hB7-2 groups. n = 4 mice per condition. The apical dendrite segment 50 to 150 μm away from the cell soma was chosen for quantification. * P < 0.05, 1-way ANOVA, post hoc Tukey’s test. Scale bar: 20 μm. 15–20 neurons/brain. Data are represented as mean ± SEM. Error bars represent SEM. See also .

Journal: The Journal of Clinical Investigation

Article Title: Human immunomodulatory ligand B7-1 mediates synaptic remodeling via the p75 neurotrophin receptor

doi: 10.1172/JCI157002

Figure Lengend Snippet: ( A ) Golgi-stained WT pyramidal neurons 3 hours after in vivo injection of hB7-1–Fc (100 ng), hB7-2–Fc (100 ng), or saline into the dSubiculum area of the hippocampal formation at P75. ( B ) There was a significant reduction in total spine density after 3 hours of hB7-1, compared with saline and the hB7-2 group. n = 4 mice/condition. ( C ) Golgi-stained p75 –/– pyramidal neurons 3 hours after in vivo injection of hB7-1–Fc (100 ng), hB7-2–Fc (100 ng), or saline into the dSubiculum area of the hippocampal formation at P75. n = 4 mice/condition ( D ) There were no significant changes in total spine density after 3 hours for the hB7-1 or hB7-2 group compared with the saline group. n = 4 mice/condition. ( E ) Golgi-stained WT pyramidal neurons 3 hours after in vivo injection of hB7-1–Fc (200 ng), hB7-2–Fc (200 ng), or saline into the dSubiculum area of the hippocampal formation at P75. ( F ) There was a significant reduction in total spine density after 3 hours of hB7-1, compared with the saline and hB7-2 groups. n = 4 mice/condition. ( G ) Golgi-stained WT pyramidal neurons 24 hours after in vivo injection of hB7-1–Fc (200 ng), hB7-2–Fc (200 ng), or saline into the dSubiculum area of the hippocampal formation at P75. ( H ) There was a significant reduction in total spine density after 24 hours of hB7-1, compared with the saline and hB7-2 groups. n = 4 mice per condition. The apical dendrite segment 50 to 150 μm away from the cell soma was chosen for quantification. * P < 0.05, 1-way ANOVA, post hoc Tukey’s test. Scale bar: 20 μm. 15–20 neurons/brain. Data are represented as mean ± SEM. Error bars represent SEM. See also .

Techniques: Staining, In Vivo, Injection, Saline

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