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marker cd31  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc marker cd31
    Marker Cd31, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 725 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/marker cd31/product/Cell Signaling Technology Inc
    Average 97 stars, based on 725 article reviews
    marker cd31 - by Bioz Stars, 2026-03
    97/100 stars

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    Cell Signaling Technology Inc antibody against cd31 #3528
    IR-Induced EndMT is Involved in the Development of RILI in vivo . (A) Representative Images of H & E-Stained Lung Tissues From a Rat Model of RILI. Scale bar = 100 μm. (B) The Expression of IL-8 in Rat Lung Tissues was Determined by Immunohistochemistry. Scale bar = 50 μm. (C) The Right Lung Tissues of the Rats Were Not Irradiated (Control Group) or Irradiated With 20 Gy X-Ray. Three Weeks after Irradiation, Lung Tissues Were Collected. Representative Images of Masson’s Trichrome-Stained Rat Lung Tissues. Scale Bar = 100 μm. (D) Representative Images Following Immunohistochemistry for <t>CD31,</t> Vimentin and α-SMA Protein Levels are Shown. (E) Western Blot Assay of VE-Cadherin and α-SMA Protein Levels. (F) Quantitative Analyses of VE-Cadherin and α-SMA Protein Levels (n = 5; Mean ± SEM; * P < 0.05 or ** P < 0.01 Compared With the Control Group; One-Way ANOVA Test of Variance)
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    Cell Signaling Technology Inc cd31 3528s
    High-throughput (HT)-compatible and nearly xeno-free synthesis of vascular networks and blood vessel organoids from fluorescently tagged human induced pluripotent stem cells (hiPSCs). A Schematic illustration of the new differentiation protocol and representative images for the main differentiation steps (scale bars: d-2, d0, d3, d5 = 100 µm; d7, d12 = 250 µm; d14, d17 = 500 µm). Created in BioRender. Skowronek, D. (2025) https://BioRender.com/e70e302 . B Shown are the steps of embedding the vascular aggregates in an Akura 96-well plate and transferring the vascular networks from the Akura 96-well plate to a PrimeSurface 96 Slit-well plate. C The use of PrimeSurface 96 Slit-well plates reduces the time required for medium exchange (left image). Akura 96-well plates allow aggregates to be embedded in small cavities, minimizing the matrix surrounding the vascular networks (black arrows) and allowing direct transfer of vascular networks (white arrows) to new plates without time-consuming manual extraction of the networks from the gel (middle and right images). D The new protocol is simple to handle and achieves high synthesis efficiency after minimal training. Shown are the efficiencies of three training runs. E The sprouting efficiency is maintained when fetal bovine serum (FBS) is replaced with human platelet lysate (hPL) or chemically defined Panexin CD (PCD). The total numbers of sufficiently sprouted networks and vascular aggregates with insufficient sprouting are written inside the bars. F,G HiPSC-derived vascular networks (F) and blood vessel organoids (G) differentiated with the HT-compatible and nearly xeno-free protocol consist of a complex network of <t>endothelial</t> cells <t>(CD31)</t> and associated pericytes (PDGFR-β) [representative images; scale bars: 50 µm ( F ); 200 µm ( G )]. White arrowheads indicate angiogenic sprouts. H Perfusion of vascular networks with TMR-amino-dextran in OrganoPlate graft plates shows anastomoses between the GFP-labeled vascular networks and the HUVEC-derived vascular bed (top, white arrowheads) as well as correct formation and permeability of the vascular networks (bottom, scale bar: 50 µm)
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    Cell Signaling Technology Inc cd31
    Identification of pericytes in CRPC, primary PCa, and normal prostate tissues via single-cell transcriptomic analysis and immunofluorescence. ( A ) t-SNE plot of 138,424 single cells originating from 13 CRPC samples, 18 treatment-naive primary PCa samples, and 6 normal prostate samples, color-coded by major cell populations. ( B ) Dot plot depicting the mean expression levels of marker genes in different cell populations. ( C - E ) Pie charts displaying the proportional distribution of eight different cell populations in normal prostate ( C ), primary PCa ( D ), and CRPC tissues ( E) . ( F ) Representative immunofluorescent images of <t>CD31</t> and α-SMA in the PCa and normal adjacent prostate specimens on a tissue microarray (scale bar: 50 μm, scale bar insets: 20 μm)
    Cd31, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti cd31 mouse mab
    Fig. 3 Histopathological findings. (A) Skin pathology in P12 showed sclerosis of the reticular dermis with excessive collagen deposition and scarce lymphocyte infiltration, but the papillary dermis and the epidermis were not affected (HE staining). (B) Scattered regenerative myofibers in P10 (HE stain ing, arrows). (C) Perivasculitis (arrow) and transmural vasculitis with an occluded lumen (arrowhead) in skeletal muscle of P4 (HE staining). (D) Prominent fascial and perivascular T lymphocytes infiltration in P4 (CD3 staining, arrows). (E) Eosinophils scattered in the fascia (E, HE staining), extending to the adjacent endomysium in P2 (F, HE staining). (F) Typical perifascicular atrophy adjacent to the inflammatory perimysium in P3 (arrows, HE staining). (G) MAC deposition on the sarcolemma of nonnecrotic myofibers and the intramuscular capillaries which were underlying the fascia in P3. (H) Vascular endothelial cells in the fascia and perifascicular endomysium was preserved in P3 <t>(CD31</t> staining). (I-L) Perifascicular MHC-I (J) and MHC-II (K) expression but without perifascicular atrophy (I, HE staining) and MxA staining (L). MAC = membrane attack complex; MHC = major histocompatibility complex class; MxA = myxovirus resistance protein
    Anti Cd31 Mouse Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc cd31 anti human antibody
    Fig. 3 Histopathological findings. (A) Skin pathology in P12 showed sclerosis of the reticular dermis with excessive collagen deposition and scarce lymphocyte infiltration, but the papillary dermis and the epidermis were not affected (HE staining). (B) Scattered regenerative myofibers in P10 (HE stain ing, arrows). (C) Perivasculitis (arrow) and transmural vasculitis with an occluded lumen (arrowhead) in skeletal muscle of P4 (HE staining). (D) Prominent fascial and perivascular T lymphocytes infiltration in P4 (CD3 staining, arrows). (E) Eosinophils scattered in the fascia (E, HE staining), extending to the adjacent endomysium in P2 (F, HE staining). (F) Typical perifascicular atrophy adjacent to the inflammatory perimysium in P3 (arrows, HE staining). (G) MAC deposition on the sarcolemma of nonnecrotic myofibers and the intramuscular capillaries which were underlying the fascia in P3. (H) Vascular endothelial cells in the fascia and perifascicular endomysium was preserved in P3 <t>(CD31</t> staining). (I-L) Perifascicular MHC-I (J) and MHC-II (K) expression but without perifascicular atrophy (I, HE staining) and MxA staining (L). MAC = membrane attack complex; MHC = major histocompatibility complex class; MxA = myxovirus resistance protein
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    Cell Signaling Technology Inc mouse anticd31
    Fig. 3 Histopathological findings. (A) Skin pathology in P12 showed sclerosis of the reticular dermis with excessive collagen deposition and scarce lymphocyte infiltration, but the papillary dermis and the epidermis were not affected (HE staining). (B) Scattered regenerative myofibers in P10 (HE stain ing, arrows). (C) Perivasculitis (arrow) and transmural vasculitis with an occluded lumen (arrowhead) in skeletal muscle of P4 (HE staining). (D) Prominent fascial and perivascular T lymphocytes infiltration in P4 (CD3 staining, arrows). (E) Eosinophils scattered in the fascia (E, HE staining), extending to the adjacent endomysium in P2 (F, HE staining). (F) Typical perifascicular atrophy adjacent to the inflammatory perimysium in P3 (arrows, HE staining). (G) MAC deposition on the sarcolemma of nonnecrotic myofibers and the intramuscular capillaries which were underlying the fascia in P3. (H) Vascular endothelial cells in the fascia and perifascicular endomysium was preserved in P3 <t>(CD31</t> staining). (I-L) Perifascicular MHC-I (J) and MHC-II (K) expression but without perifascicular atrophy (I, HE staining) and MxA staining (L). MAC = membrane attack complex; MHC = major histocompatibility complex class; MxA = myxovirus resistance protein
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    Image Search Results


    IR-Induced EndMT is Involved in the Development of RILI in vivo . (A) Representative Images of H & E-Stained Lung Tissues From a Rat Model of RILI. Scale bar = 100 μm. (B) The Expression of IL-8 in Rat Lung Tissues was Determined by Immunohistochemistry. Scale bar = 50 μm. (C) The Right Lung Tissues of the Rats Were Not Irradiated (Control Group) or Irradiated With 20 Gy X-Ray. Three Weeks after Irradiation, Lung Tissues Were Collected. Representative Images of Masson’s Trichrome-Stained Rat Lung Tissues. Scale Bar = 100 μm. (D) Representative Images Following Immunohistochemistry for CD31, Vimentin and α-SMA Protein Levels are Shown. (E) Western Blot Assay of VE-Cadherin and α-SMA Protein Levels. (F) Quantitative Analyses of VE-Cadherin and α-SMA Protein Levels (n = 5; Mean ± SEM; * P < 0.05 or ** P < 0.01 Compared With the Control Group; One-Way ANOVA Test of Variance)

    Journal: Dose-Response

    Article Title: NEDD4-Mediated Endothelial-Mesenchymal Transition Participates in Radiation-Induced Lung Injury Through the ATM Signaling Pathway

    doi: 10.1177/15593258251352726

    Figure Lengend Snippet: IR-Induced EndMT is Involved in the Development of RILI in vivo . (A) Representative Images of H & E-Stained Lung Tissues From a Rat Model of RILI. Scale bar = 100 μm. (B) The Expression of IL-8 in Rat Lung Tissues was Determined by Immunohistochemistry. Scale bar = 50 μm. (C) The Right Lung Tissues of the Rats Were Not Irradiated (Control Group) or Irradiated With 20 Gy X-Ray. Three Weeks after Irradiation, Lung Tissues Were Collected. Representative Images of Masson’s Trichrome-Stained Rat Lung Tissues. Scale Bar = 100 μm. (D) Representative Images Following Immunohistochemistry for CD31, Vimentin and α-SMA Protein Levels are Shown. (E) Western Blot Assay of VE-Cadherin and α-SMA Protein Levels. (F) Quantitative Analyses of VE-Cadherin and α-SMA Protein Levels (n = 5; Mean ± SEM; * P < 0.05 or ** P < 0.01 Compared With the Control Group; One-Way ANOVA Test of Variance)

    Article Snippet: Antibody against CD31 (#3528) was purchased from Cell Signaling Technology (Beverly, MA, USA).

    Techniques: In Vivo, Staining, Expressing, Immunohistochemistry, Irradiation, Control, Western Blot

    IR-Induced Lung EndMT Accompanies the Development of RILI in vitro . (A) HUVECs Were Exposed to 0 or 10 Gy X-rays. The Tube-formation Capacity of HUVECs was Investigated at 2 h after Irradiation. Scale Bar = 500 μm. (B) HUVECs Were Exposed to 0, 2, 5 or 10 Gy X-rays. Representative Images Showing the Cell Morphology are provided at 72 h after Irradiation. Scale Bar = 200 μm. (C) HUVECs Were Exposed to 0 or 10 Gy X-rays. The Cell Morphology was Observed at 24, 48 and 72 h After Irradiation. Scale bar = 200 μm. (D) HUVECs Were Exposed to 0, 2, 5 or 10 Gy X-rays. The Distribution of Phalloidin in HUVECs was Detected by Immunofluorescence at 72 h after Irradiation. Scale bar = 20 μm. (E) HUVECs Were Exposed to 0 or 10 Gy X-rays. The Distribution of Phalloidin in HUVECs was Detected at 0.5, 6, 24, 48 and 72 h after Irradiation. Scale Bar = 20 μm. (F) HUVECs Were Exposed to 0, 2, 5 or 10 Gy X-Rays. The Protein Expression of Vimentin, α-SMA and CD31 in HUVECs was Examined by Western Blot at 72 h after Irradiation. (G) Quantitative Analyses of CD31, Vimentin and α-SMA Protein Levels (n = 3; Mean ± SEM; * P < 0.05 or ** P < 0.01 Compared With the Control Group; One-Way ANOVA Test of Variance). (H) HUVECs Were Exposed to 0 or 10 Gy X-rays. The Protein Expression of EndMT-Related Markers in HUVECs was Detected at 0.5, 6, 24, 48 and 72 h after Irradiation. (I) Quantitative Analyses of CD31, Vimentin and α-SMA Protein Levels (n = 3; Mean ± SEM; * P < 0.05 or ** P < 0.01 Compared With the Control Group; One-Way ANOVA Test of Variance). (J) HUVECs Were Exposed to 0, 2, 5 or 10 Gy X-rays. The Expression of CD31 was Examined by Immunofluorescence at 72 h After Irradiation. Scale Bar = 20 μm. (K) HUVECs Were Exposed to 0 or 10 Gy X-rays. The Expression of CD31 was Examined at 0.5, 6, 24, 48 and 72 h After Irradiation. Scale Bar = 20 μm

    Journal: Dose-Response

    Article Title: NEDD4-Mediated Endothelial-Mesenchymal Transition Participates in Radiation-Induced Lung Injury Through the ATM Signaling Pathway

    doi: 10.1177/15593258251352726

    Figure Lengend Snippet: IR-Induced Lung EndMT Accompanies the Development of RILI in vitro . (A) HUVECs Were Exposed to 0 or 10 Gy X-rays. The Tube-formation Capacity of HUVECs was Investigated at 2 h after Irradiation. Scale Bar = 500 μm. (B) HUVECs Were Exposed to 0, 2, 5 or 10 Gy X-rays. Representative Images Showing the Cell Morphology are provided at 72 h after Irradiation. Scale Bar = 200 μm. (C) HUVECs Were Exposed to 0 or 10 Gy X-rays. The Cell Morphology was Observed at 24, 48 and 72 h After Irradiation. Scale bar = 200 μm. (D) HUVECs Were Exposed to 0, 2, 5 or 10 Gy X-rays. The Distribution of Phalloidin in HUVECs was Detected by Immunofluorescence at 72 h after Irradiation. Scale bar = 20 μm. (E) HUVECs Were Exposed to 0 or 10 Gy X-rays. The Distribution of Phalloidin in HUVECs was Detected at 0.5, 6, 24, 48 and 72 h after Irradiation. Scale Bar = 20 μm. (F) HUVECs Were Exposed to 0, 2, 5 or 10 Gy X-Rays. The Protein Expression of Vimentin, α-SMA and CD31 in HUVECs was Examined by Western Blot at 72 h after Irradiation. (G) Quantitative Analyses of CD31, Vimentin and α-SMA Protein Levels (n = 3; Mean ± SEM; * P < 0.05 or ** P < 0.01 Compared With the Control Group; One-Way ANOVA Test of Variance). (H) HUVECs Were Exposed to 0 or 10 Gy X-rays. The Protein Expression of EndMT-Related Markers in HUVECs was Detected at 0.5, 6, 24, 48 and 72 h after Irradiation. (I) Quantitative Analyses of CD31, Vimentin and α-SMA Protein Levels (n = 3; Mean ± SEM; * P < 0.05 or ** P < 0.01 Compared With the Control Group; One-Way ANOVA Test of Variance). (J) HUVECs Were Exposed to 0, 2, 5 or 10 Gy X-rays. The Expression of CD31 was Examined by Immunofluorescence at 72 h After Irradiation. Scale Bar = 20 μm. (K) HUVECs Were Exposed to 0 or 10 Gy X-rays. The Expression of CD31 was Examined at 0.5, 6, 24, 48 and 72 h After Irradiation. Scale Bar = 20 μm

    Article Snippet: Antibody against CD31 (#3528) was purchased from Cell Signaling Technology (Beverly, MA, USA).

    Techniques: In Vitro, Irradiation, Immunofluorescence, Expressing, Western Blot, Control

    NEDD4 Participates in EndMT in Endothelial Cells. (A) NEDD4 Protein Levels in NEDD4 - Overexpressing HUVECs. (B) Quantitative Analyses of NEDD4 Protein Level (n = 3; Mean SEM; ** P < 0.01 Compared With the Control Group; t test of Variance). (C) NEDD4 Overexpression Reduced the Tube-formation Capacity of HUVECs. Scale Bar = 500 μm. (D) Phase-Contrast Micrographs of Control and NEDD4-Overexpressing HUVECs. Scale Bar = 200 μm. (E–H) CD31 and Vimentin Protein Expression in Control and NEDD4-Overexpressing HUVECs (n = 3; Mean ± SEM; * P < 0.05 or ** P < 0.01 Compared With the Control Group; t test of Variance)

    Journal: Dose-Response

    Article Title: NEDD4-Mediated Endothelial-Mesenchymal Transition Participates in Radiation-Induced Lung Injury Through the ATM Signaling Pathway

    doi: 10.1177/15593258251352726

    Figure Lengend Snippet: NEDD4 Participates in EndMT in Endothelial Cells. (A) NEDD4 Protein Levels in NEDD4 - Overexpressing HUVECs. (B) Quantitative Analyses of NEDD4 Protein Level (n = 3; Mean SEM; ** P < 0.01 Compared With the Control Group; t test of Variance). (C) NEDD4 Overexpression Reduced the Tube-formation Capacity of HUVECs. Scale Bar = 500 μm. (D) Phase-Contrast Micrographs of Control and NEDD4-Overexpressing HUVECs. Scale Bar = 200 μm. (E–H) CD31 and Vimentin Protein Expression in Control and NEDD4-Overexpressing HUVECs (n = 3; Mean ± SEM; * P < 0.05 or ** P < 0.01 Compared With the Control Group; t test of Variance)

    Article Snippet: Antibody against CD31 (#3528) was purchased from Cell Signaling Technology (Beverly, MA, USA).

    Techniques: Control, Over Expression, Expressing

    High-throughput (HT)-compatible and nearly xeno-free synthesis of vascular networks and blood vessel organoids from fluorescently tagged human induced pluripotent stem cells (hiPSCs). A Schematic illustration of the new differentiation protocol and representative images for the main differentiation steps (scale bars: d-2, d0, d3, d5 = 100 µm; d7, d12 = 250 µm; d14, d17 = 500 µm). Created in BioRender. Skowronek, D. (2025) https://BioRender.com/e70e302 . B Shown are the steps of embedding the vascular aggregates in an Akura 96-well plate and transferring the vascular networks from the Akura 96-well plate to a PrimeSurface 96 Slit-well plate. C The use of PrimeSurface 96 Slit-well plates reduces the time required for medium exchange (left image). Akura 96-well plates allow aggregates to be embedded in small cavities, minimizing the matrix surrounding the vascular networks (black arrows) and allowing direct transfer of vascular networks (white arrows) to new plates without time-consuming manual extraction of the networks from the gel (middle and right images). D The new protocol is simple to handle and achieves high synthesis efficiency after minimal training. Shown are the efficiencies of three training runs. E The sprouting efficiency is maintained when fetal bovine serum (FBS) is replaced with human platelet lysate (hPL) or chemically defined Panexin CD (PCD). The total numbers of sufficiently sprouted networks and vascular aggregates with insufficient sprouting are written inside the bars. F,G HiPSC-derived vascular networks (F) and blood vessel organoids (G) differentiated with the HT-compatible and nearly xeno-free protocol consist of a complex network of endothelial cells (CD31) and associated pericytes (PDGFR-β) [representative images; scale bars: 50 µm ( F ); 200 µm ( G )]. White arrowheads indicate angiogenic sprouts. H Perfusion of vascular networks with TMR-amino-dextran in OrganoPlate graft plates shows anastomoses between the GFP-labeled vascular networks and the HUVEC-derived vascular bed (top, white arrowheads) as well as correct formation and permeability of the vascular networks (bottom, scale bar: 50 µm)

    Journal: Angiogenesis

    Article Title: High-throughput differentiation of human blood vessel organoids reveals overlapping and distinct functions of the cerebral cavernous malformation proteins

    doi: 10.1007/s10456-025-09985-5

    Figure Lengend Snippet: High-throughput (HT)-compatible and nearly xeno-free synthesis of vascular networks and blood vessel organoids from fluorescently tagged human induced pluripotent stem cells (hiPSCs). A Schematic illustration of the new differentiation protocol and representative images for the main differentiation steps (scale bars: d-2, d0, d3, d5 = 100 µm; d7, d12 = 250 µm; d14, d17 = 500 µm). Created in BioRender. Skowronek, D. (2025) https://BioRender.com/e70e302 . B Shown are the steps of embedding the vascular aggregates in an Akura 96-well plate and transferring the vascular networks from the Akura 96-well plate to a PrimeSurface 96 Slit-well plate. C The use of PrimeSurface 96 Slit-well plates reduces the time required for medium exchange (left image). Akura 96-well plates allow aggregates to be embedded in small cavities, minimizing the matrix surrounding the vascular networks (black arrows) and allowing direct transfer of vascular networks (white arrows) to new plates without time-consuming manual extraction of the networks from the gel (middle and right images). D The new protocol is simple to handle and achieves high synthesis efficiency after minimal training. Shown are the efficiencies of three training runs. E The sprouting efficiency is maintained when fetal bovine serum (FBS) is replaced with human platelet lysate (hPL) or chemically defined Panexin CD (PCD). The total numbers of sufficiently sprouted networks and vascular aggregates with insufficient sprouting are written inside the bars. F,G HiPSC-derived vascular networks (F) and blood vessel organoids (G) differentiated with the HT-compatible and nearly xeno-free protocol consist of a complex network of endothelial cells (CD31) and associated pericytes (PDGFR-β) [representative images; scale bars: 50 µm ( F ); 200 µm ( G )]. White arrowheads indicate angiogenic sprouts. H Perfusion of vascular networks with TMR-amino-dextran in OrganoPlate graft plates shows anastomoses between the GFP-labeled vascular networks and the HUVEC-derived vascular bed (top, white arrowheads) as well as correct formation and permeability of the vascular networks (bottom, scale bar: 50 µm)

    Article Snippet: To confirm endothelial differentiation, cells were fixed with 4% PFA at passage 1 and stained for the endothelial markers CD31 (Cell Signaling, 3528S, 1:800), VE-cadherin (2500S, 1:400, Cell Signaling) and VWF (Thermo Fisher Scientific, MA5-14029, 1:66).

    Techniques: High Throughput Screening Assay, Transferring, Extraction, Derivative Assay, Labeling, Permeability

    Perfusion of blood vessel organoids (BVO) on chorioallantoic membranes (CAM). A Schematic illustration of the perfusion approach. Created in BioRender. Skowronek, D. (2025) https://BioRender.com/n06n764 . B Shown are blood vessel organoids cultivated on the CAM associated with chicken blood vessels. The pictures were taken on day 1 and day 6 (scale bars = 2 mm). C Sectioning and H&E staining demonstrated nucleated chicken erythrocytes within the vascular structures of the blood vessel organoid (black arrow head) (upper scale bar = 500 µm; bottom scale bar = 25 µm). D The expression of CD31 (upper image) and PDGFR-β (lower image) were verified by immunohistochemistry staining (brown) (scale bar = 100 µm)

    Journal: Angiogenesis

    Article Title: High-throughput differentiation of human blood vessel organoids reveals overlapping and distinct functions of the cerebral cavernous malformation proteins

    doi: 10.1007/s10456-025-09985-5

    Figure Lengend Snippet: Perfusion of blood vessel organoids (BVO) on chorioallantoic membranes (CAM). A Schematic illustration of the perfusion approach. Created in BioRender. Skowronek, D. (2025) https://BioRender.com/n06n764 . B Shown are blood vessel organoids cultivated on the CAM associated with chicken blood vessels. The pictures were taken on day 1 and day 6 (scale bars = 2 mm). C Sectioning and H&E staining demonstrated nucleated chicken erythrocytes within the vascular structures of the blood vessel organoid (black arrow head) (upper scale bar = 500 µm; bottom scale bar = 25 µm). D The expression of CD31 (upper image) and PDGFR-β (lower image) were verified by immunohistochemistry staining (brown) (scale bar = 100 µm)

    Article Snippet: To confirm endothelial differentiation, cells were fixed with 4% PFA at passage 1 and stained for the endothelial markers CD31 (Cell Signaling, 3528S, 1:800), VE-cadherin (2500S, 1:400, Cell Signaling) and VWF (Thermo Fisher Scientific, MA5-14029, 1:66).

    Techniques: Staining, Expressing, Immunohistochemistry

    Structural defects in KO vascular networks. A Immunofluorescence staining for CD31 (endothelial marker, green) and PDGFR-β (pericyte marker, red) indicated a reduced correlation between ECs and pericytes in CCM1, CCM2, and CCM3 KO vascular networks (scale bar: 100 µm). Correlation was evaluated by using the Pearson’s correlation coefficient (r) calculated with the JACoP ImageJ plugin. B , C Immunofluorescence staining for ZO-1 (B) and VE-cadherin ( C ) revealed irregular tight and adherens junctions in CCM1 , CCM2, and CCM3 KO vascular networks (Alexa 647; scale bars: 25 µm). Statistical analyses demonstrated a significant reduction of Alexa 647 (ZO-1) fluorescence intensity in CCM2 and CCM3 KO networks. Data are presented as individual data points and means. Multiple two-sample t-tests with Welch's correction and Holm-Šídák adjustment for multiple testing were used for statistical analyses (* = Padj < 0.05)

    Journal: Angiogenesis

    Article Title: High-throughput differentiation of human blood vessel organoids reveals overlapping and distinct functions of the cerebral cavernous malformation proteins

    doi: 10.1007/s10456-025-09985-5

    Figure Lengend Snippet: Structural defects in KO vascular networks. A Immunofluorescence staining for CD31 (endothelial marker, green) and PDGFR-β (pericyte marker, red) indicated a reduced correlation between ECs and pericytes in CCM1, CCM2, and CCM3 KO vascular networks (scale bar: 100 µm). Correlation was evaluated by using the Pearson’s correlation coefficient (r) calculated with the JACoP ImageJ plugin. B , C Immunofluorescence staining for ZO-1 (B) and VE-cadherin ( C ) revealed irregular tight and adherens junctions in CCM1 , CCM2, and CCM3 KO vascular networks (Alexa 647; scale bars: 25 µm). Statistical analyses demonstrated a significant reduction of Alexa 647 (ZO-1) fluorescence intensity in CCM2 and CCM3 KO networks. Data are presented as individual data points and means. Multiple two-sample t-tests with Welch's correction and Holm-Šídák adjustment for multiple testing were used for statistical analyses (* = Padj < 0.05)

    Article Snippet: To confirm endothelial differentiation, cells were fixed with 4% PFA at passage 1 and stained for the endothelial markers CD31 (Cell Signaling, 3528S, 1:800), VE-cadherin (2500S, 1:400, Cell Signaling) and VWF (Thermo Fisher Scientific, MA5-14029, 1:66).

    Techniques: Immunofluorescence, Staining, Marker, Fluorescence

    Identification of pericytes in CRPC, primary PCa, and normal prostate tissues via single-cell transcriptomic analysis and immunofluorescence. ( A ) t-SNE plot of 138,424 single cells originating from 13 CRPC samples, 18 treatment-naive primary PCa samples, and 6 normal prostate samples, color-coded by major cell populations. ( B ) Dot plot depicting the mean expression levels of marker genes in different cell populations. ( C - E ) Pie charts displaying the proportional distribution of eight different cell populations in normal prostate ( C ), primary PCa ( D ), and CRPC tissues ( E) . ( F ) Representative immunofluorescent images of CD31 and α-SMA in the PCa and normal adjacent prostate specimens on a tissue microarray (scale bar: 50 μm, scale bar insets: 20 μm)

    Journal: Cancer Cell International

    Article Title: Pericytes in castration-resistant prostate cancer associated with disease progression and immunotherapy response: insights from single-cell analysis

    doi: 10.1186/s12935-025-03838-3

    Figure Lengend Snippet: Identification of pericytes in CRPC, primary PCa, and normal prostate tissues via single-cell transcriptomic analysis and immunofluorescence. ( A ) t-SNE plot of 138,424 single cells originating from 13 CRPC samples, 18 treatment-naive primary PCa samples, and 6 normal prostate samples, color-coded by major cell populations. ( B ) Dot plot depicting the mean expression levels of marker genes in different cell populations. ( C - E ) Pie charts displaying the proportional distribution of eight different cell populations in normal prostate ( C ), primary PCa ( D ), and CRPC tissues ( E) . ( F ) Representative immunofluorescent images of CD31 and α-SMA in the PCa and normal adjacent prostate specimens on a tissue microarray (scale bar: 50 μm, scale bar insets: 20 μm)

    Article Snippet: In the present investigation, we employed the following primary antibodies for immunofluorescence: α-SMA (1:2000, #19245, Cell Signaling Technology, Danvers, MA, USA), CD31 (1:1000, #3528, Cell Signaling Technology).

    Techniques: Immunofluorescence, Expressing, Marker, Microarray

    Fig. 3 Histopathological findings. (A) Skin pathology in P12 showed sclerosis of the reticular dermis with excessive collagen deposition and scarce lymphocyte infiltration, but the papillary dermis and the epidermis were not affected (HE staining). (B) Scattered regenerative myofibers in P10 (HE stain ing, arrows). (C) Perivasculitis (arrow) and transmural vasculitis with an occluded lumen (arrowhead) in skeletal muscle of P4 (HE staining). (D) Prominent fascial and perivascular T lymphocytes infiltration in P4 (CD3 staining, arrows). (E) Eosinophils scattered in the fascia (E, HE staining), extending to the adjacent endomysium in P2 (F, HE staining). (F) Typical perifascicular atrophy adjacent to the inflammatory perimysium in P3 (arrows, HE staining). (G) MAC deposition on the sarcolemma of nonnecrotic myofibers and the intramuscular capillaries which were underlying the fascia in P3. (H) Vascular endothelial cells in the fascia and perifascicular endomysium was preserved in P3 (CD31 staining). (I-L) Perifascicular MHC-I (J) and MHC-II (K) expression but without perifascicular atrophy (I, HE staining) and MxA staining (L). MAC = membrane attack complex; MHC = major histocompatibility complex class; MxA = myxovirus resistance protein

    Journal: Arthritis research & therapy

    Article Title: Clinicopathological profile of eosinophilic fasciitis: a retrospective cohort study from a neuromuscular disorder center in China.

    doi: 10.1186/s13075-025-03574-z

    Figure Lengend Snippet: Fig. 3 Histopathological findings. (A) Skin pathology in P12 showed sclerosis of the reticular dermis with excessive collagen deposition and scarce lymphocyte infiltration, but the papillary dermis and the epidermis were not affected (HE staining). (B) Scattered regenerative myofibers in P10 (HE stain ing, arrows). (C) Perivasculitis (arrow) and transmural vasculitis with an occluded lumen (arrowhead) in skeletal muscle of P4 (HE staining). (D) Prominent fascial and perivascular T lymphocytes infiltration in P4 (CD3 staining, arrows). (E) Eosinophils scattered in the fascia (E, HE staining), extending to the adjacent endomysium in P2 (F, HE staining). (F) Typical perifascicular atrophy adjacent to the inflammatory perimysium in P3 (arrows, HE staining). (G) MAC deposition on the sarcolemma of nonnecrotic myofibers and the intramuscular capillaries which were underlying the fascia in P3. (H) Vascular endothelial cells in the fascia and perifascicular endomysium was preserved in P3 (CD31 staining). (I-L) Perifascicular MHC-I (J) and MHC-II (K) expression but without perifascicular atrophy (I, HE staining) and MxA staining (L). MAC = membrane attack complex; MHC = major histocompatibility complex class; MxA = myxovirus resistance protein

    Article Snippet: Serial frozen sections of the muscle and fascia specimens were stained with hematoxylin and eosin (HE), anti- major histocompatibility complex class (MHC)-I rabbit monoclonal antibody (mAb, clone EP1395Y; Abcam), anti-MHC-II mouse mAb (clone CR3/43; Dako), anti-C5b-9 (MAC) mouse mAb (clone aE11; Dako), and anti-myxovirus resistance protein (MxA) rabbit polyclonal antibody (ab95926; Abcam), anti-CD3 mouse mAb (clone LN10; Zhongshan Golden Bridge Biotechnology), anti-CD4 mouse mAb (clone ZM-0418; Zhongshan Golden Bridge Biotechnology), anti-CD8 rabbit mAb (clone SP16; Zhongshan Golden Bridge Biotechnology), anti-CD68 rabbit mAb (clone KP1; Zhongshan Golden Bridge Biotechnology), anti-CD31 mouse mAb (3528 S, Cell Signaling Technology).

    Techniques: Staining, H&E Stain, Expressing, Membrane, Immunopeptidomics