cd105 antibody, anti-human  (Miltenyi Biotec)

Journal: Blood Vessels, Thrombosis & Hemostasis

Article Title: Resilience of the bone marrow vascular architecture to aging and hematological stress

doi: 10.1016/j.bvth.2026.100156

Figure Lengend Snippet: The architecture of CD31 hi vessels in murine femora is highly conserved. (A) Femora from young adult naïve, aged, and blood-let mice were excised, benzoic acid benzyl ester-cleared, imaged by LSFM in stitched tile scans, and the resulting 3D data sets segmented for CD31 hi and CD105 + vasculature. (B-D) Quantitative analysis of the CD31 hi vasculature in 5 young adult male mice (n = 5). (B) Distribution of branch hierarchy levels with a Gaussian-like peak at level 14. (C) Branch length distribution peaking at ∼100 μm with extending to 3000 μm. (D) Branch diameter distribution ranging from 9 μm to 70 μm, peaking at 19 μm. (E-G) Quantitative analysis of the CD31 hi vasculature in 5 young adult female mice (n = 5), same as (B-D) for male mice. (H) 3D reconstruction of the CD31 hi vasculature for the young mice shown in panels B-G demonstrating high structural conservation. Scale bar, 1 mm. An overlay of all 5 male vessel trees is shown in .

Article Snippet: CD105 + vessels were segmented in Imaris and skeletonized to assess parameters such as vessel volume, vessel-vessel distance, branch length, and branching degree.

Techniques:

Journal: Blood Vessels, Thrombosis & Hemostasis

Article Title: Resilience of the bone marrow vascular architecture to aging and hematological stress

doi: 10.1016/j.bvth.2026.100156

Figure Lengend Snippet: CD105 + vessels exhibit conserved architecture and proximal narrowing in young mice. (A) Representative midshaft section of CD105 + vasculature (green) in a young naïve male mouse. Bottom row: fluorescence intensity, segmented surface, skeletonized tree, and the vessel-to-vessel distance map (200-μm section). Skeleton (cyan), end points (blue), and branching points (red). Gray outline indicates marrow boundary. Scale bars, 500 μm. (B-D) Distribution of (B) vessel diameter, (C) branching angle, and (D) vessel-to-vessel spacing in young naïve male (top) and female (bottom) mice (n = 5 per sex). See “Methods” and for detailed results. (E-J) Regional analyses along the femoral shaft divided into 9 overlapping tiles (see ). Distribution of local values of (E) vessel diameter, (F) branching angle, and (G) vessel-to-vessel distance in representative hip, mid, and knee regions of the shaft. The top row shows results of male mice, the bottom row of female mice. (H-J) Averaged values of (H) vessel diameter, (I) branching angle, and (J) vessel-to-vessel distance for each region: hip-proximal (yellow), midshaft (magenta), and knee-proximal (grape). Filled bars represent male mice, lighter colored shaded bars female mice. Shown are mean ± SEM. SEM, standard error of the mean.

Article Snippet: CD105 + vessels were segmented in Imaris and skeletonized to assess parameters such as vessel volume, vessel-vessel distance, branch length, and branching degree.

Techniques: Fluorescence

Journal: Blood Vessels, Thrombosis & Hemostasis

Article Title: Resilience of the bone marrow vascular architecture to aging and hematological stress

doi: 10.1016/j.bvth.2026.100156

Figure Lengend Snippet: Morphological differences in CD105 + small vessels of aged vs young mice. (A-B) Representative midshaft femur sections from an aged male (A) and a young, blood-let mouse (B), showing segmented CD105 + surfaces and skeletonized vasculature. Color coding as in . Scale bar, 500 μm. (C-E) Distribution of vessel diameters along the femoral shaft. (F-H) Mean vessel diameter per region along the femur. (I-K) Distribution of vessel-to-vessel distances. (L-N) Regional mean vessel-to-vessel distances. Dashed lines and lighter shaded bars indicate female data. See for further details.

Article Snippet: CD105 + vessels were segmented in Imaris and skeletonized to assess parameters such as vessel volume, vessel-vessel distance, branch length, and branching degree.

Techniques:

Journal: Blood Vessels, Thrombosis & Hemostasis

Article Title: Resilience of the bone marrow vascular architecture to aging and hematological stress

doi: 10.1016/j.bvth.2026.100156

Figure Lengend Snippet: Regional changes in the CD105 + microvascular complexity along the femur. (A) Fraction of long branches (>100 μm) in young naïve (blue), blood-let (red), and aged (gray) mice (filled symbols, male; open symbols, females). (B) Proportion of vessels running parallel to the central vein. (C) Fraction of vessels with diameters <25 μm. (D) Ratio of vessel segments to branching points. (E) Ratio of end points to branching points. (F) Fraction of branching points with ≥4 outgoing branches, only branches longer than 25 μm and branching degree ≥3 were included. All data shown as mean ± SEM. SEM, standard error of the mean.

Article Snippet: CD105 + vessels were segmented in Imaris and skeletonized to assess parameters such as vessel volume, vessel-vessel distance, branch length, and branching degree.

Techniques:

Journal: Blood Vessels, Thrombosis & Hemostasis

Article Title: Resilience of the bone marrow vascular architecture to aging and hematological stress

doi: 10.1016/j.bvth.2026.100156

Figure Lengend Snippet: Modest increased MK volume in aged male mice. (A) Representative midshaft section showing CD105 + MKs (magenta) in a young adult male mouse. Bottom row: fluorescence intensity, segmented surface, MK outlines, and MK-vessel distance map (200-μm section). MK outlines and distance transform shown for a single slice. Gray outline indicates marrow boundary. Scale bar, 500 μm. (B-D) Quantification of MK properties in young (blue), aged (gray), and blood-let (red) mice (filled symbols: males; open symbols: females). (B) MK-to-AF volume ratio; (C) MK surface-to-volume ratio; and (D) proportion of MK surface within 5 μm of a vessel. (E-G) MK-vessel distance distributions; dashed lines: female mice. (H-J) Regional mean MK-vessel distances for hip, mid, and knee. Lighter colored shaded bars: females. All data shown as mean ± SEM. See “Methods” and and for details. BM, bone marrow; SEM, standard error of the mean; Sur./Vol., surface/volume.

Article Snippet: CD105 + vessels were segmented in Imaris and skeletonized to assess parameters such as vessel volume, vessel-vessel distance, branch length, and branching degree.

Techniques: Fluorescence

Journal: bioRxiv

Article Title: Human SHED-derived extracellular cues activate a specialized neuroprotective and regenerative program in developing retinal ganglion cells

doi: 10.64898/2026.06.25.733625

Figure Lengend Snippet: (a) Immunofluorescence staining showing expression of Vimentin (green) and CD105 (red) in DPSC and SHED compared with HaCaT epithelial controls. (b) STRO-1 (green) immunostaining in SHED. Nuclei were counterstained with DAPI (blue). Scale bar = 100μm (c) Representative flow cytometry analyses demonstrating expression of mesenchymal stem cell markers (CD73, CD90, CD105, HLA-ABC) and absence of hematopoietic markers (CD34, CD45). All experiments were perfomed at passage 5 (d) Growth curves comparing cumulative population doublings of DPSC and SHED derived from four independent donors across serial passages. SHED displayed enhanced proliferative capacity and reduced donor-to-donor variability.

Article Snippet: Antibodies against the following human antigens were used: CD105-FITC (Miltenyi Biotect, Bergisch Gladbach, Germany, cat# 130-112-327, 1:50), CD90-FITC (Miltenyi Biotec, cat# 130-114-901, 1:50), CD44-VioBlue (Miltenyi Biotec, cat# 130-113-906, 1:50), CD73-APC (Miltenyi Biotec, cat# 130-111-909, 1:50), MSC Phenotyping Cocktail-PE (CD34, CD14, CD19, CD45, Miltenyi Biotec cat# 130-125-285, dilution according to the manufacturer’s instructions).

Techniques: Immunofluorescence, Staining, Expressing, Immunostaining, Flow Cytometry, Derivative Assay

Journal: iScience

Article Title: LDLRAD2 drives glycolysis and angiogenesis to promote extramedullary infiltration in acute myeloid leukemia

doi: 10.1016/j.isci.2026.115987

Figure Lengend Snippet: EMI-AML patients are characterized by elevated LDLRAD2 expression, increased MVD, and increased glycolytic protein levels (A) Representative IHC staining of bone marrow biopsy samples from AML patients revealed higher expression of LDLRAD2 in EMI-AML patients than in controls. (B) Quantitative analysis of the percentage of LDLRAD2-positive cells measured from IHC staining. (C) Representative IHC staining of the glycolysis-related proteins LDHA and PKM2 in bone marrow biopsy samples from AML patients and controls. (D) Quantitative analysis of the percentage of LDHA-positive and PKM2-positive cells measured from IHC staining. (E) Representative IHC staining of bone marrow biopsy samples from AML patients revealed increased MVD in EMI-AML patients than in controls. (F) Quantitative analysis of MVD, presented as both the percentage of CD31-positive and CD105-positive cells measured from IHC staining. The original magnification was 200×; scale bars, 50 μm. Data are presented as mean ± SD. Representative images are shown from one control specimen, one non-EMI specimen, and three EMI specimens. Quantification was performed from three representative fields per bone marrow biopsy specimen. B, D, and F were analyzed by one-way ANOVA followed by Tukey’s multiple-comparison test; for D and F, statistical analyses were performed separately for each marker. ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus control; # p < 0.05, ## p < 0.01 and ### p < 0.001 versus non-EMI. Scale bars, 50 μm. Arrows indicate positive cells. EMI, extramedullary infiltration.

Article Snippet: After standard deparaffinization and antigen retrieval, tissue sections were incubated with primary antibodies against LDLRAD2 (Thermo Fisher, USA), LDHA (Wanleibio, China), PKM2 (Zenbio, China), CD105 (Abclonal, China), CD31 (Zenbio, China), CD34 (Abclonal, China), and CD117 (Wanleibio, China), followed by appropriate HRP-conjugated secondary antibody (Thermo Fisher, USA) and DAB (Maixinbio, China) chromogenic development, with hematoxylin (Solarbio, China) counterstaining.

Techniques: Expressing, Immunohistochemistry, Control, Comparison, Marker

Journal: iScience

Article Title: LDLRAD2 drives glycolysis and angiogenesis to promote extramedullary infiltration in acute myeloid leukemia

doi: 10.1016/j.isci.2026.115987

Figure Lengend Snippet: LDLRAD2 drives EMI in vivo by activating the MTDH/PI3K/AKT pathway to promote glycolysis and angiogenesis (Part 2) (A) Representative images of IHC staining for CD31 and CD105 expression at an original magnification of 400×. Scale bars, 50 μm. The arrows indicate positive cells. (B) Quantification of the percentage of CD31-positive and CD105-positive cells measured from IHC staining. (C) TUNEL staining revealed a significant increase in the number of apoptotic cells in the spleens of the mice injected with LV-sh LDLRAD2 -transfected HL-60 cells compared with that observed in the control mice; original magnification of 400×. Scale bars, 50 μm. The arrows indicate tumor cells. (D) Percentage of TUNEL-positive cells. (E) Western blot analysis revealed downregulated LDLRAD2, MTDH, p-PI3K, p -AKT, p -mTOR, LDHA, and PKM2 expression in the spleens of LDLRAD2 -knockdown mice, thereby indicating the suppression of the MTDH/PI3K/AKT signaling pathway and glycolysis. (F) The schematic illustrates the mechanisms of LDLRAD2 in EMI of AML via MTDH/PI3K/AKT signaling. Protein expression was measured via western blotting, and β-actin was used as a loading control. Data are presented as mean ± SD. B and D were analyzed by one-way ANOVA followed by Tukey’s multiple-comparison test using three biologically independent mice per group; in B, CD31 and CD105 were analyzed separately. E shows representative western blots of spleen lysates. ∗∗∗ p < 0.001 versus control. Scale bars, 50 μm. Arrows indicate positive cells or TUNEL-positive cells. NC, negative control (continued from ).

Article Snippet: After standard deparaffinization and antigen retrieval, tissue sections were incubated with primary antibodies against LDLRAD2 (Thermo Fisher, USA), LDHA (Wanleibio, China), PKM2 (Zenbio, China), CD105 (Abclonal, China), CD31 (Zenbio, China), CD34 (Abclonal, China), and CD117 (Wanleibio, China), followed by appropriate HRP-conjugated secondary antibody (Thermo Fisher, USA) and DAB (Maixinbio, China) chromogenic development, with hematoxylin (Solarbio, China) counterstaining.

Techniques: In Vivo, Immunohistochemistry, Expressing, TUNEL Assay, Staining, Injection, Transfection, Control, Western Blot, Knockdown, Comparison, Negative Control

Journal: bioRxiv

Article Title: PS FAD mutants and γ-secretase inhibition accumulate VEGFR2-derived peptide VCTF1 suppressing brain VEGFR2 dimerization, angiogenesis and neuroprotection

doi: 10.64898/2026.05.12.724648

Figure Lengend Snippet: (A) , Wild-type (WT) and KI mice HTRZ for either PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were infused with vehicle (0.2% BSA in PBS) or VEGF-A (a total of 3.5μg in 100μl of vehicle) through the carotid artery for 15 days using a mini osmotic pump as in Methods. Left: Brain coronal sections (40μm thick) were prepared and immunostained with anti-Col IV antibodies to visualize brain vessels. Enhanced visualization surfaces were generated using Imaris software from representative confocal images of ipsilateral hemispheres. Scale bar: 50μm. Right: Graph shows total vessel length density in WT and PS1 FAD brains quantified using Imaris 9.9 software as in Methods. (B) , WT and HTRZ for PS1 FAD mutants M146V or I213T mice were injected through the carotid artery for 20 minutes with either vehicle or 100ng of VEGF-A in vehicle prepared as in 1A using a catheter as described in Methods. Brain microvessels (MV) were isolated as in Methods, lysed in Triton X-100 buffer, and subjected to immunoprecipitation (IP) with anti-VEGFR2 antibody or control IgG. Left: IPs were analyzed on Western blots (WBs) using anti-endoglin or anti-VEGFR2 antibodies (upper panel). Input samples are shown in lower panel. β-actin: loading control. Right: Graph shows quantification of endoglin co-IPed with VEGFR2, normalized to IPed VEGFR2. (C) , WT mice were infused for 15 days through the carotid artery with vehicle or VEGF-A in vehicle as in 1A using a mini osmotic pump (as in 1A). For RO injection, mice were treated with vehicle (2% DMSO, 30% PEG 300, 5% Tween-80 in ddH2O) or RO in vehicle (5mg/kg body weight) via five injections in tail vein one injection every three days, with first injection administered 1 hour before osmotic pump implantation. Brain coronal sections (40μm) were prepared and immunostained with anti-Col IV antibodies as in 1A. Left: Representative confocal images of ipsilateral hemispheres are shown prepared as in 1A. Scale bar: 50μm. Right: Graph shows total vessel length density quantified using Imaris software as in 1A. (D) , WT adult mice were treated with either 50μl vehicle as in 1C or 1mg/kg RO in vehicle via carotid artery as in Methods. 15-16 hrs later, 50 μl vehicle prepared as in 1A or 100ng VEGF-A in vehicle was administered via carotid artery for 10-20 minutes using a catheter as in 1B. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. Vinculin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (E) , WT mice and mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T) were treated with vehicle or VEGF-A via carotid artery for 10-20 minutes using a catheter as in 1D. Brain MVs were isolated and extracted as in 1B. Left: p-VEGFR2 (Tyr1054/Tyr1059), VEGFR2, p-ERK1/2 and ERK1/2 are detected on WBs of extracts with specific antibodies in MV extracts. β-actin: loading control. Right: Graphs show fold change of phosphorylated to total protein ratio. (F) , WT pCECs were prepared and treated as in Methods with vehicle (DMSO) or RO (200nM in DMSO) and then stimulated with either vehicle (PBS) or VEGF-A (20ng in PBS) for 15min. Upper: Cells were co-immunostained with either anti-VEGFR2 antibodies (green) or early endosome marker Rab5 (red) and cell nuclei were stained with Hoechst (blue) as in Methods. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in RO-treated WT cells compared to vehicle-treated cells measured with Imaris software. (G) , pCECs from either WT or mice HTRZ for PS1 FAD mutant M146V (WT/M146V) or I213T (WT/I213T), were stimulated with vehicle or VEGF-A in vehicle as in 1F. Upper: Cells were co-stained with anti-VEGFR2 antibodies and early endosome marker Rab5 as in 1F. Cell nuclei were stained with Hoechst (blue) as in 1F. Yellow fluorescence in merged images indicates co-localization of VEGFR2 with Rab5. Scale bar 0.5μm. Lower: Graph shows percent of VEGFR2 co-localized with Rab5 in PS1 FAD WT/M146V or WT/I213T HTRZ mice compared to WT measured with Imaris software. For Figs A-G, data are shown as Mean ± S.E. from at least three independent experiments or as indicated in the dot plots. Statistical analysis was performed using two-way ANOVA followed by Tukey post-hoc test. ns = not significant, *p<0.05, **p<0.01, ***p<0.001.

Article Snippet: Mouse monoclonal anti-Flag tag (M2; F1804) was from Millipore Sigma, anti-GAPDH (2118S) from Cell Signaling Technologies (Beverly, MA), anti-VEGFR2 (OTI12C1) from Origene, anti-endoglin (CD-105; NBP2-22122) and anti-LAMP2 (NBP2-22217) from Novus Biologicals, Inc, anti-Rab5 (D-11) and anti-Rab7 (B-3) from Santa Cruz Biotechnology, Inc. Chicken polyclonal anti-GFAP (ab4674) was from Abcam.

Techniques: Mutagenesis, Generated, Software, Injection, Isolation, Immunoprecipitation, Control, Western Blot, Marker, Staining, Fluorescence

Journal: bioRxiv

Article Title: PS FAD mutants and γ-secretase inhibition accumulate VEGFR2-derived peptide VCTF1 suppressing brain VEGFR2 dimerization, angiogenesis and neuroprotection

doi: 10.64898/2026.05.12.724648

Figure Lengend Snippet: (A), Brain tissue extracts were prepared as in Methods from twelve PS1 FAD patients each carrying a different PS1 mutation, and twelve non-demented controls described in Methods. Left: VEGFR2 dimers and monomers were detected in brain extracts on WBs using anti-VEGFR2 antibody D5B1. Representative gels with control (C1-4) or FAD samples (FAD1-4) expressing mutants P264L, A260V, N135S and P242H respectively are shown. Vinculin: loading control. Right: Graph shows the fold change in VEGFR2 dimer to monomer ratio of FAD and control samples. (B), Brain tissue extract from control and PS1 FAD patient brains described in 7A were prepared and IPed with anti-endoglin antibody (ab252345) or IgG as in Methods. Upper panel: VEGFR2 co-IPed with endoglin was detected on WBs using an anti-VEGFR2 antibody as in 7A. Lower panel: Input samples are shown. Representative gel with control samples (C1, C2) and FAD samples (FAD1, FAD2) expressing mutants A260V and P264L respectively is shown. β-actin: loading control. Right: Graph shows relative levels of VEGFR2 co-precipitated with endoglin. (C), Brain sections from control and PS1 FAD patients were prepared as in Methods and stained for Col IV as in 1A. Upper: Representative images show brain vessels in either PS1 FAD or control (CT) brain sections. Scale bar: 80μm. Lower: Graph shows total vessel length density in PS1 FAD and CT brains quantified with Imaris software as in 1A. A-C , bars represent Mean ± S.E. For statistical analysis, unpaired t-test was performed. *p < 0.05, **p<0.01 and ***p<0.001.

Article Snippet: Mouse monoclonal anti-Flag tag (M2; F1804) was from Millipore Sigma, anti-GAPDH (2118S) from Cell Signaling Technologies (Beverly, MA), anti-VEGFR2 (OTI12C1) from Origene, anti-endoglin (CD-105; NBP2-22122) and anti-LAMP2 (NBP2-22217) from Novus Biologicals, Inc, anti-Rab5 (D-11) and anti-Rab7 (B-3) from Santa Cruz Biotechnology, Inc. Chicken polyclonal anti-GFAP (ab4674) was from Abcam.

Techniques: Mutagenesis, Control, Expressing, Staining, Software

Journal: Cells

Article Title: Alterations in Circulating Progenitor Cell Composition in Rheumatoid Arthritis

doi: 10.3390/cells15080726

Figure Lengend Snippet: CD235a + and CD45 − CD31 − stromal cells circulating in peripheral blood. ( a ) CD45/CD31 dot plot showing populations 16, 17, 18, 19 and 20. ( b ) UMAP shows the size of each cluster, and ( c ) TriMAP shows the relative cluster location. CD45/CD31 plots highlighting the expression of ( d ) CD235a, ( e ) CD133, ( f ) CD34 and ( g ) CD105. The intensity scale indicates high expression of the marker in red. Frequency of ( h ) Pop 20, ( i ) Pop 17, and ( j ) Pop 18. Mann-Whitney test. Dot plots showing the expression of ( k ) CD34/CD133, ( l ) CD271/ CD105, and CD90 with ( m ) CD105, ( n ) CD271, and ( o ) PDPN in Pop 16 and Pop 19. Frequency of ( p ) Pop 16 and ( q ) Pop 19. t -test for Pop 16; Mann–Whitney test for Pop 19. All dot plots show mean and SD, n = 12 RA and 9 HC.

Article Snippet: CD105 , VioBlue-A , 130-099-666 , Miltenyi Biotec , 1/100 , V3.

Techniques: Expressing, Marker, MANN-WHITNEY