mouse serum  (R&D Systems)

Journal: Blood Vessels, Thrombosis & Hemostasis

Article Title: An angiopoietin-2 vaccine improves arteriovenous malformation pathology in hereditary hemorrhagic telangiectasia mice

doi: 10.1016/j.bvth.2026.100155

Figure Lengend Snippet: Immunogenicity of the ANG2-P3:CRM197 vaccine in C57BL/6 mice. (A) Schematic diagram of the vaccination schedule and generation of the BMP9/10ib model (created with biorender.com ). (B) Protein sequence alignment of the C-terminal end of human ANG2 (hANG2), mouse ANG2 (mANG2), human ANG1 (hANG1), and mouse ANG1 (mANG1), along with the peptide sequences of ANG2-P3 and ANG1-P3. (C-D) Serum antibody titers against ANG2-P3 (C) and ANG1-P3 (D) in ANG2-P3:CRM197-vaccinated females (Vac-1 to Vac-5) and controls (injected with saline [Sal-1 and Sal-2] or CRM197-only [CRM-1 to CRM-5]). The vaccinated females with the highest anti-ANG2-P3 titers were identified as “best responders” (marked with a red box). OD, optical density.

Article Snippet: After 3 additional washes with PBST, serial dilutions of individual mouse serum samples were prepared, along with a reference mouse anti-BMP9 antibody (no. MAB3209; R&D Systems) and a reference mouse anti-BMP10 antibody (no. MAB2926; R&D Systems), both diluted in 1% BSA in PBS.

Techniques: Immunopeptidomics, Sequencing, Injection, Saline

Journal: Blood Vessels, Thrombosis & Hemostasis

Article Title: An angiopoietin-2 vaccine improves arteriovenous malformation pathology in hereditary hemorrhagic telangiectasia mice

doi: 10.1016/j.bvth.2026.100155

Figure Lengend Snippet: ANG2-P3:CRM197 vaccine reduces AVM pathology in BMP9/10ib neonates. (A) Serum antibody titers against ANG2-P3 in pups and their corresponding dams vaccinated with ANG2-P3:CRM197 (Vac-1 to Vac-3) or injected with saline (Saline). Vac-1, Vac-2, and Vac-3 pups: n = 7; Saline pups: n = 2. Dams: n = 1. (B) Representative immunofluorescence staining with isolectin B4 (IB4; green) and of SMA (red) in P6 retinas of pups treated with PBS or BMP9/10ib from a dam vaccinated with ANG2-P3:CRM197 or injected with saline. Scale bar: 1.5 mm. (C-D ) AVM count per retina (C), and retinal AVM surface area (D) in BMP9/10ib pups from dams vaccinated with ANG2-P3:CRM197 or injected with saline (Saline). BMP9/10ib + saline: n = 24; BMP9/10ib + ANG2-P3:CRM197: n = 37 (C). BMP9/10ib + saline: n = 24; BMP9/10ib + ANG2-P3:CRM197: n = 34 (D). (E) Spearman rank correlation matrix of the indicated variables (n = 15). (F-H) Retinal artery diameter (F), retinal vein diameter (G), and SMA coverage area (H) in BMP9/10ib pups from dams vaccinated with ANG2-P3:CRM197 or injected with saline (Saline). Data are shown as mean ± standard error of the mean (SEM); unpaired t test with Welch correction for panel C, Mann-Whitney test for panel D, and 1-way analysis of variance with Tukey multiple comparisons test for panels F-H. PBS + saline: n = 15; BMP9/10ib + saline: n = 24; BMP9/10ib + ANG2-P3:CRM197: n = 37 (F,G). PBS + saline: n = 13; BMP9/10ib + saline: n = 21; BMP9/10ib + ANG2-P3:CRM197: n = 29 (H). ∗ P < .05; ∗∗∗ P ≤ .001; ∗∗∗∗ P < .0001. (I) Immunoassay data measuring ANG2 levels in plasma from patients with HHT and healthy controls. Data are shown as mean ± SEM; unpaired t test with Welch correction. Healthy: n = 36; HHT: n = 36. ∗∗ P ≤ .01. a, artery; ns, not significant; v, vein.

Article Snippet: After 3 additional washes with PBST, serial dilutions of individual mouse serum samples were prepared, along with a reference mouse anti-BMP9 antibody (no. MAB3209; R&D Systems) and a reference mouse anti-BMP10 antibody (no. MAB2926; R&D Systems), both diluted in 1% BSA in PBS.

Techniques: Injection, Saline, Immunofluorescence, Staining, MANN-WHITNEY, Clinical Proteomics

Journal: International Dental Journal

Article Title: Pulpitis Transiently Affect Hepatic Bone Morphogenetic Protein 9 Expression by Lipopolysaccharide

doi: 10.1016/j.identj.2026.109435

Figure Lengend Snippet: Changes of BMP9 expression in liver after pulp opening in rats/mice. (A) Haematoxylin–eosin (HE) staining of mice pulpitis tissues (black arrows: inflammatory cell). (B) Expression of BMP9 in rat liver occurred mainly in the peripheral cells of the sinusoid (blue arrows); it decreased significantly at D1 and returned to normal at D3 and D7 (IHC). (C) At D1 after pulp opening, the expression of BMP9 in mice liver of the PO group decreased significantly, but there was no significant change in the PC or AN groups (blue arrows) (IHC). (D) At D3 after pulp opening, the expression of BMP9 in liver tissue of mice in PO group increased, returning to the normal level, whereas there was no significant change in other groups (IHC). (E) RT-qPCR results showed that BMP9 gene expression began to decline at 6 hours after pulp opening and reached its lowest level at D1, before returning to normal levels. (F and G) WB results showed that the expression of BMP9 protein decreased at D1 after pulp opening and increased at D3. (H) ELISA showed that BMP9 levels in the blood of mice decreased at D1 and rose at D3. AN, anaesthetic; D, day; NS, normal sample; PC, pulp capping; PO, pulp opening. Data are presented as mean ± SD; n = 6; * P < .05. Black scale: 100 μm, red scale: 50 μm; green scale: 150 μm; white scale: 25 μm.

Article Snippet: The slides were incubated overnight at 4°C with antibodies against BMP9 (1:500, sc-514211, Santa Cruz Biotechnology) and LPS (1:100, KL20041-01, KangLang Biological).

Techniques: Expressing, Staining, Quantitative RT-PCR, Gene Expression, Enzyme-linked Immunosorbent Assay

Journal: International Dental Journal

Article Title: Pulpitis Transiently Affect Hepatic Bone Morphogenetic Protein 9 Expression by Lipopolysaccharide

doi: 10.1016/j.identj.2026.109435

Figure Lengend Snippet: Changes of LPS concentration in liver and blood of mice after pulp opening and BMP9 expression in mHSCs stimulated by P.g LPS. The concentration of LPS in the blood (A) and liver (B) began to rise at 12 hours, peaking at D1 and dropping to basal level at D3 (ELISA and IHC) ( n = 6). (C) The expression sites of BMP9 (yellow) and demsin (green) overlapped in liver tissue (IF) ( n = 3). (D and E) P.g LPS inhibited the expression of BMP9 in mHSCs cultured in vitro for a short time (WB) ( n = 3). D, day; NS, normal sample. Data are presented as mean ± SD; * P < .05; ** P < .01. Black scale: 100 μm, red scale: 50 μm; white scale: 50 μm.

Article Snippet: The slides were incubated overnight at 4°C with antibodies against BMP9 (1:500, sc-514211, Santa Cruz Biotechnology) and LPS (1:100, KL20041-01, KangLang Biological).

Techniques: Concentration Assay, Expressing, Enzyme-linked Immunosorbent Assay, Cell Culture, In Vitro

Journal: International Dental Journal

Article Title: Pulpitis Transiently Affect Hepatic Bone Morphogenetic Protein 9 Expression by Lipopolysaccharide

doi: 10.1016/j.identj.2026.109435

Figure Lengend Snippet: UNC0642 inhibited the downregulation of BMP9 expression in P.g LPS-stimulated mHSCs in vitro. (A) P.g LPS inhibited the expression of BMP9 and increased the H3K9me2 levels. UNC0642 at different molar concentrations restored the expression of BMP9 and inhibited H3K9me2 levels (WB). (B) The changes in BMP9 expression. (C) The changes in H3K9me2 levels. (D-I) P.g LPS reduced the fluorescence intensity of BMP9 and increased that of H3K9me2. 1 μM UNC0642 restored the fluorescence intensity of BMP9 and inhibited that of H3K9me2 (ICF). me2: dimethylation. Data are presented as mean ± SD; n = 3; ** P < .01.

Article Snippet: The slides were incubated overnight at 4°C with antibodies against BMP9 (1:500, sc-514211, Santa Cruz Biotechnology) and LPS (1:100, KL20041-01, KangLang Biological).

Techniques: Expressing, In Vitro, Fluorescence

Journal: International Dental Journal

Article Title: Pulpitis Transiently Affect Hepatic Bone Morphogenetic Protein 9 Expression by Lipopolysaccharide

doi: 10.1016/j.identj.2026.109435

Figure Lengend Snippet: UNC0642 restored BMP9 expression in C57 mice and binding of H3K9me2 to the promoter region of BMP9 gene. (A) The expression of BMP9 in the DMSO-PO group was decreased, whereas that in the UNC0642-PO group was upregulated and similar to that in the DMSO control group (WB). (B) The RT-qPCR results are consistent with the IHC results. (C and D) The WB results were consistent with the IHC results ( n = 6). The groups 1 to 3 correspond to the DMSO group, DMSO-PO group, and UNC0642-PO group, respectively. (E) After stimulation of mHSCs with P.g LPS, the enrichment rate of H3K9me2 in the promoter region of BMP9 gene was significantly increased (ChIP) ( n = 3). (F) Full-text pattern diagram. LPS from pulpitis reached the liver through the bloodstream, stimulating hepatic stellate cells and regulating the expression of BMP9 in the liver via H3K9 dimethylation. DMSO represents the working fluid of inhibitors in vivo: DMSO + 40% PEG300 + 5% Tween80 + double-distilled H2O; LPS, samples stimulated with P.g LPS; me2, dimethylation; NS, normal sample; PO, pulp opening. Data are presented as mean ± SD; * P < .05. Black scale: 100 μm, white scale: 50 μm.

Article Snippet: The slides were incubated overnight at 4°C with antibodies against BMP9 (1:500, sc-514211, Santa Cruz Biotechnology) and LPS (1:100, KL20041-01, KangLang Biological).

Techniques: Expressing, Binding Assay, Control, Quantitative RT-PCR, In Vivo

Journal: bioRxiv

Article Title: Physiological perfusion of human vasculature reveals a YAP/TAZ-Apelin switch linking intraluminal flow to endothelial state transitions and vessel remodeling

doi: 10.64898/2026.03.21.713033

Figure Lengend Snippet: (A) Vascular beds on Day 4 which were grown from ENG - or ALK1 -knockdown endothelial cells or treated with 10 ng/mL BMP9 (ERG: endothelial nuclei, CD31: vessels). (B) Quantification of (A) (10 devices per condition across 4 independent experiments for shRNA vessels; 6 devices per condition across 2 independent experiments for BMP9 treatments). (C) Particle image velocimetry analysis showing velocity magnitude for ENG -knockdown, ALK1 -knockdown, and BMP9-treated vessels on Day 4. (D) Quantification of (C) (42-45 vessels and 6 devices per condition across 2 independent experiments). (E) Gene set scoring of endothelial cells on Day 4 from the scRNA-seq experiment. Scores are for BMP9 up/down-regulated genes from Al Tabosh et al . . Endothelial cells are divided by either cell type (i.e. T1 or T2), predicted labels from Goveia et al . (i.e. tip cell or stalk-like), or experimental condition (i.e. low or high flow). Cohen’s d effect sizes are shown. (F) Correlation coefficients between gene set scoring of BMP9 up/down-regulated genes (Al Tabosh et al .), VEGFA up/down-regulated genes (Zhang et al ., ), and YAP/TAZ targets. Adjusted p-values were calculated using a permutation test followed by Bonferroni correction. (G) Gene set scoring of BMP9 down-regulated genes and VEGFA up-regulated genes. (H) Gene set scoring of BMP9 up-regulated genes and VEGFA down-regulated genes. (I) Log2 fold change rank plot showing a subset of markers genes for the T1 cell type (left). Gene set scoring for the subset of marker genes (right). (F-H) All endothelial cells from the scRNA-seq dataset were used. (J) Heatmap of qPCR gene expression from monolayer BMVECs treated with BMP9 (10 ng/mL) and/or VEGFA (100 ng/mL) for 48 hrs (3 independent experiments). (K) Images of ENG - or ALK1 -knockdown vascular beds on Day 4 treated with 100 nM Axitinib (CD31: vessels). (L) Quantification of (K) (6 devices per condition across 2 independent experiments). (B, D, L) 2-tailed unpaired Welch’s t-test (* p < 0.05; ** p < 0.01; *** p < 0.001). (B, L) Error bars show SEM.

Article Snippet: Human recombinant BMP9 (R&D Systems; 10 ng/mL) and/or human recombinant VEGF-165 (Gibco; 100 ng/mL) were added for 48 hrs.

Techniques: Knockdown, shRNA, Marker, Gene Expression

Journal: bioRxiv

Article Title: Physiological perfusion of human vasculature reveals a YAP/TAZ-Apelin switch linking intraluminal flow to endothelial state transitions and vessel remodeling

doi: 10.64898/2026.03.21.713033

Figure Lengend Snippet: (A) Evaluation of shRNA knockdown efficiency (2 independent experiments). (B) ERG and MKI67 immunostainings of vascular beds on Day 4 which were grown from shRNA-treated endothelial cells or additionally treated with BMP9 (10 ng/mL). (C) Quantifications of (B) (6 devices per condition across 2 independent experiments). 2-tailed unpaired student’s t-test (ns: not significant). (A, C) Error bars show SEM.

Article Snippet: Human recombinant BMP9 (R&D Systems; 10 ng/mL) and/or human recombinant VEGF-165 (Gibco; 100 ng/mL) were added for 48 hrs.

Techniques: shRNA, Knockdown

Journal: bioRxiv

Article Title: Physiological perfusion of human vasculature reveals a YAP/TAZ-Apelin switch linking intraluminal flow to endothelial state transitions and vessel remodeling

doi: 10.64898/2026.03.21.713033

Figure Lengend Snippet: (A) Gene Set Enrichment Analysis of VIVOS scRNA-seq data for BMP9 up/down-regulated genes (Al Tabosh et al. , ). (B) Left: Venn diagram between BMP9 down-regulated genes (Al Tabosh et al. ) and VEGFA up-regulated genes (Zhang et al. , ). Right: Gene set scoring of VIVOS scRNA-seq data for BMP9 down-regulated genes and VEGFA up-regulated genes, with overlapping genes removed. Endothelial cells from all conditions are shown. (C) Gene set scoring of the human tumor angiogenesis atlas from Goveia et al. for BMP9 down-regulated genes and VEGFA up-regulated genes. (D) Gene set scoring of VIVOS scRNA-seq data for BMP9 up/down-regulated genes and YAP/TAZ targets. T1 endothelial cells on Day 4 are shown. (E) Gene set scoring of VIVOS scRNA-seq data for BMP9 down-regulated genes and VEGFA up-regulated genes. Endothelial cells from Day 1 are shown. RNA velocity streamlines (left). Individual gene expressions (right). (F) Rank plot of differentially expressed genes for tip cell and stalk-like human atlas clusters. (G) Heatmap of qPCR gene expression from monolayer BMVECs treated with BMP9 (10 ng/mL) and/or VEGFA (100 ng/mL) for 48 hrs. Numbers represent average relative expressions from 3 independent experiments. “Mean expression” refers to the geometric mean of the 7 individual genes. (H) Mean expression values from (G). (I) VEGFR1 and VEGFR2 expressions from the same experiment as (G). (J) VEGFR1 expression in endothelial cells from all conditions. (K) Proposed model for antagonization of VEGFA-induced transcription by BMP9. (B-E) Spearman’s correlation coefficient. (H-I) 2-tailed unpaired student’s t-test (* p < 0.05; ** p < 0.01; *** p < 0.001). Error bars show SEM.

Article Snippet: Human recombinant BMP9 (R&D Systems; 10 ng/mL) and/or human recombinant VEGF-165 (Gibco; 100 ng/mL) were added for 48 hrs.

Techniques: Gene Expression, Expressing