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R&D Systems human recombinant bmp9

(A) Vascular beds on Day 4 which were grown from ENG - or ALK1 -knockdown endothelial cells or treated with 10 ng/mL <t>BMP9</t> (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.

Human Recombinant Bmp9, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 44 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 95 stars, based on 44 article reviews

human recombinant bmp9 - by Bioz Stars, 2026-07

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1) Product Images from "Physiological perfusion of human vasculature reveals a YAP/TAZ-Apelin switch linking intraluminal flow to endothelial state transitions and vessel remodeling"

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

Journal: bioRxiv

doi: 10.64898/2026.03.21.713033

(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.

Figure Legend 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.

Techniques Used: Knockdown, shRNA, Marker, Gene Expression

(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.

Figure Legend 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.

Techniques Used: shRNA, Knockdown

(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.

Figure Legend 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.

Techniques Used: Gene Expression, Expressing

Image Search Results

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

Effects of silencing the AQP1 gene and exogenous administration of BMP9 on AQP1 and BMP/TGF‐β signaling molecules in human pulmonary microvascular endothelial cells. HPMECs were silenced for the AQP1 gene and the relative mRNA and protein expression of AQP1 (A, B), BMPR2 (C, D), TGFBR1 (E, F), and TGFB1 (G, H) were estimated before and after the exogenous administration of BMP9. Relative mRNA expression is shown in dot plots (dots, individual values; line in the middle, median values; lower and upper lines, 25th and 75th percentiles) (A, n = 6; C, n = 7; E, n = 7; G, n = 6). Protein expression was analyzed by SDS‐PAGE and immunoblotting, and relative expression was estimated by densitometry using β‐tubulin as a loading control. Relative protein expression is shown with bar plots (mean ± SEM; dots, individual values) (B, n = 4; D, n = 4; F, n = 4; H, n = 4). Representative expression of AQP1 (B), BMPR2 (D), TGFBR1 (F), and TGFB1 (H) (upper panels) and β‐tubulin (lower panels) proteins in the AQP1 ‐silenced HPMEC homogenates. Specificity (siRNA negative control), efficiency ( AQP1 siRNA), and the effect of BMP9 exogenous administration on the non‐transfected controls were tested each time to ensure the consistency and reproducibility across the independent experiments. Statistical analysis was performed using the Mann–Whitney test. *, p < 0.05; **, p < 0.01 compared to the non‐transfected control HPMECs.

Journal: Comprehensive Physiology

Article Title: Disrupting BMP / TGF ‐β Signaling: Modulation of AQP1 and TGFB1 in Human Pulmonary Microvascular Endothelial Cells

doi: 10.1002/cph4.70066

Figure Lengend Snippet: Effects of silencing the AQP1 gene and exogenous administration of BMP9 on AQP1 and BMP/TGF‐β signaling molecules in human pulmonary microvascular endothelial cells. HPMECs were silenced for the AQP1 gene and the relative mRNA and protein expression of AQP1 (A, B), BMPR2 (C, D), TGFBR1 (E, F), and TGFB1 (G, H) were estimated before and after the exogenous administration of BMP9. Relative mRNA expression is shown in dot plots (dots, individual values; line in the middle, median values; lower and upper lines, 25th and 75th percentiles) (A, n = 6; C, n = 7; E, n = 7; G, n = 6). Protein expression was analyzed by SDS‐PAGE and immunoblotting, and relative expression was estimated by densitometry using β‐tubulin as a loading control. Relative protein expression is shown with bar plots (mean ± SEM; dots, individual values) (B, n = 4; D, n = 4; F, n = 4; H, n = 4). Representative expression of AQP1 (B), BMPR2 (D), TGFBR1 (F), and TGFB1 (H) (upper panels) and β‐tubulin (lower panels) proteins in the AQP1 ‐silenced HPMEC homogenates. Specificity (siRNA negative control), efficiency ( AQP1 siRNA), and the effect of BMP9 exogenous administration on the non‐transfected controls were tested each time to ensure the consistency and reproducibility across the independent experiments. Statistical analysis was performed using the Mann–Whitney test. *, p < 0.05; **, p < 0.01 compared to the non‐transfected control HPMECs.

Article Snippet: HPMECs were treated with BMP9 (5 ng/mL) (OriGene, Rockville, MD, USA) 24 h post‐transfection.

Techniques: Expressing, SDS Page, Western Blot, Control, Negative Control, Transfection, MANN-WHITNEY

Effects of silencing the TGFB1 gene and exogenous administration of BMP9 on BMP/TGF‐β signaling molecules and AQP1 in human pulmonary microvascular endothelial cells. HPMECs were silenced for the TGFB1 gene and the relative mRNA and protein expression of TGFB1 (A, B), TGFBR1 (C, D), AQP1 (E, F), and BMPR2 (G, H) were estimated before and after the exogenous administration of BMP9. Relative mRNA expression is shown in dot plots (dots, individual values; line in the middle, median values; lower and upper lines, 25th and 75th percentiles) (A, n = 5; C, n = 6; E, n = 4; G, n = 7). Protein expression was analyzed by SDS‐PAGE and immunoblotting, and relative expression was estimated by densitometry using β‐tubulin or Actin as a loading control. Relative protein expression is shown with bar plots (mean ± SEM; dots, individual values) (B, n = 4; D, n = 7; F, n = 4; H, n = 6). Representative expression of TGFB1 (B), TGFBR1 (D), AQP1 (F), and BMPR2 (H) (upper panels) and β‐tubulin (lower panels) proteins in the TGFB1 ‐silenced HPMEC homogenates. Specificity (siRNA negative control), efficiency ( TGFB1 siRNA), and the effect of BMP9 exogenous administration on the non‐transfected controls were tested each time to ensure consistency and reproducibility across the independent experiments. Statistical analysis was performed using the Mann–Whitney test. *, p < 0.05; **, p < 0.01 compared to the non‐transfected control HPMECs.

Journal: Comprehensive Physiology

Article Title: Disrupting BMP / TGF ‐β Signaling: Modulation of AQP1 and TGFB1 in Human Pulmonary Microvascular Endothelial Cells

doi: 10.1002/cph4.70066

Figure Lengend Snippet: Effects of silencing the TGFB1 gene and exogenous administration of BMP9 on BMP/TGF‐β signaling molecules and AQP1 in human pulmonary microvascular endothelial cells. HPMECs were silenced for the TGFB1 gene and the relative mRNA and protein expression of TGFB1 (A, B), TGFBR1 (C, D), AQP1 (E, F), and BMPR2 (G, H) were estimated before and after the exogenous administration of BMP9. Relative mRNA expression is shown in dot plots (dots, individual values; line in the middle, median values; lower and upper lines, 25th and 75th percentiles) (A, n = 5; C, n = 6; E, n = 4; G, n = 7). Protein expression was analyzed by SDS‐PAGE and immunoblotting, and relative expression was estimated by densitometry using β‐tubulin or Actin as a loading control. Relative protein expression is shown with bar plots (mean ± SEM; dots, individual values) (B, n = 4; D, n = 7; F, n = 4; H, n = 6). Representative expression of TGFB1 (B), TGFBR1 (D), AQP1 (F), and BMPR2 (H) (upper panels) and β‐tubulin (lower panels) proteins in the TGFB1 ‐silenced HPMEC homogenates. Specificity (siRNA negative control), efficiency ( TGFB1 siRNA), and the effect of BMP9 exogenous administration on the non‐transfected controls were tested each time to ensure consistency and reproducibility across the independent experiments. Statistical analysis was performed using the Mann–Whitney test. *, p < 0.05; **, p < 0.01 compared to the non‐transfected control HPMECs.

Article Snippet: HPMECs were treated with BMP9 (5 ng/mL) (OriGene, Rockville, MD, USA) 24 h post‐transfection.

Techniques: Expressing, SDS Page, Western Blot, Control, Negative Control, Transfection, MANN-WHITNEY

Effects of silencing the TGFB1 gene and exogenous administration of BMP9 on BMP/TGF‐β ligands in human pulmonary microvascular endothelial cells. HPMECs were silenced for the TGFB1 gene, and the relative mRNA and protein expression of BMP9 (A, B) and BMP10 (C, D) were estimated. BMP10 expression was estimated before and after the exogenous administration of BMP9. Relative mRNA expression is shown in dot plots (dots, individual values; line in the middle, median values; lower and upper lines, 25th and 75th percentiles) (A, n = 6; C, n = 5). Protein expression was analyzed by SDS‐PAGE and immunoblotting, and relative expression was estimated by densitometry using β‐tubulin or Actin as a loading control. Relative protein expression is shown with bar plots (mean ± SEM; dots, individual values) (B, n = 4; D, n = 5). Representative expression of BMP9 (B), and BMP10 (D) (upper panels) and β‐tubulin/Actin (lower panels) proteins in the TGFB1 ‐silenced HPMEC homogenates. Specificity (siRNA negative control), efficiency ( TGFB1 siRNA), and the effect of BMP9 exogenous administration on the non‐transfected controls were tested each time to ensure consistency and reproducibility across the independent experiments. Statistical analysis was performed using the Mann–Whitney test. *, p < 0.05 compared to the non‐transfected control HPMECs.

Journal: Comprehensive Physiology

Article Title: Disrupting BMP / TGF ‐β Signaling: Modulation of AQP1 and TGFB1 in Human Pulmonary Microvascular Endothelial Cells

doi: 10.1002/cph4.70066

Figure Lengend Snippet: Effects of silencing the TGFB1 gene and exogenous administration of BMP9 on BMP/TGF‐β ligands in human pulmonary microvascular endothelial cells. HPMECs were silenced for the TGFB1 gene, and the relative mRNA and protein expression of BMP9 (A, B) and BMP10 (C, D) were estimated. BMP10 expression was estimated before and after the exogenous administration of BMP9. Relative mRNA expression is shown in dot plots (dots, individual values; line in the middle, median values; lower and upper lines, 25th and 75th percentiles) (A, n = 6; C, n = 5). Protein expression was analyzed by SDS‐PAGE and immunoblotting, and relative expression was estimated by densitometry using β‐tubulin or Actin as a loading control. Relative protein expression is shown with bar plots (mean ± SEM; dots, individual values) (B, n = 4; D, n = 5). Representative expression of BMP9 (B), and BMP10 (D) (upper panels) and β‐tubulin/Actin (lower panels) proteins in the TGFB1 ‐silenced HPMEC homogenates. Specificity (siRNA negative control), efficiency ( TGFB1 siRNA), and the effect of BMP9 exogenous administration on the non‐transfected controls were tested each time to ensure consistency and reproducibility across the independent experiments. Statistical analysis was performed using the Mann–Whitney test. *, p < 0.05 compared to the non‐transfected control HPMECs.

Article Snippet: HPMECs were treated with BMP9 (5 ng/mL) (OriGene, Rockville, MD, USA) 24 h post‐transfection.

Techniques: Expressing, SDS Page, Western Blot, Control, Negative Control, Transfection, MANN-WHITNEY

( A ) Schematic diagram of the vaccination schedule and generation of the BMP9/10ib model. ( 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 and 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.

Journal: bioRxiv

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

doi: 10.1101/2025.10.13.682178

Figure Lengend Snippet: ( A ) Schematic diagram of the vaccination schedule and generation of the BMP9/10ib model. ( 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 and 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: The anti-BMP9 and anti-BMP10 antibody ELISAs were performed as follows: 96-well ELISA plates (Maxisorp, Nunc) were coated with 100 μL per well of recombinant BMP9 (3209-BP-010, R&D Systems) or BMP10 (2926-BP-025, R&D Systems) at 1 μg/mL in a coating buffer (15 mM K2HPO4, 25 mM KH2PO4, 0.1 M NaCl, 0.1 mM EDTA, and 7.5 mM NaN3), and incubated overnight at 4°C.

Techniques: Sequencing, Injection, Saline

( 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). ( B ) Representative immunofluorescence staining with isolectin B4 (IB4, green) and of α-smooth muscle actin (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. a, artery; v, vein. Scale bar, 1.5 mm. ( C and 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). ( E ) Spearman’s rank correlation matrix of the indicated variables. ( 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 meanLJ±LJs.e.m.; unpaired t-test with Welch’s correction (C), Mann-Whitney test (D), and one-way ANOVA with Tukey’s multiple comparisons test (F-H). ns, not significant; * P < 0.05; *** P ≤ 0.001; **** P < 0.0001.

Journal: bioRxiv

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

doi: 10.1101/2025.10.13.682178

Figure Lengend Snippet: ( 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). ( B ) Representative immunofluorescence staining with isolectin B4 (IB4, green) and of α-smooth muscle actin (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. a, artery; v, vein. Scale bar, 1.5 mm. ( C and 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). ( E ) Spearman’s rank correlation matrix of the indicated variables. ( 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 meanLJ±LJs.e.m.; unpaired t-test with Welch’s correction (C), Mann-Whitney test (D), and one-way ANOVA with Tukey’s multiple comparisons test (F-H). ns, not significant; * P < 0.05; *** P ≤ 0.001; **** P < 0.0001.

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

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