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R&D Systems anti human bmp10
Anti Human Bmp10, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti human bmp10/product/R&D Systems
Average 93 stars, based on 16 article reviews

anti human bmp10 - by Bioz Stars, 2026-05

93/100 stars

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BMP10 ameliorates LPS-induced acute lung injury and inflammation. A H&E staining of lung sections demonstrated that BMP10 treatment mitigated LPS-induced thickening of the alveolar septal walls, reduced infiltration of inflammatory cells within the interstitium, and preserved the alveolar structure; Scale bar, 100 μm. B LPS-stimulated mice treated with BMP10 exhibited a significantly lower lung injury score compared with the LPS group ( *p < 0.05, n = 4 mice per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). C IF staining of BALF indicated that BMP10 treatment significantly decreased the recruitment of activated neutrophils into the alveolar space induced by LPS ( *p < 0.05, n = 4 mice per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test); Scale bar, 50 µm; Red, MPO; Green, Ly6G; Blue, DAPI; D The levels of proinflammatory cytokines, including TNFα and IL-6, in the BALF, blood, and pulmonary homogenate supernatants were significantly lower in BMP10-treated, LPS-stimulated mice compared with the LPS-stimulated mice group ( *p < 0.05, n = 3—5 mice per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). BMP10 bone morphogenetic protein 10, H&E hematoxylin and eosin, LPS lipopolysaccharide, IF immunofluorescence, BALF bronchoalveolar lavage fluid, TNF-α tumor necrosis factor alpha, MPO myeloperoxidase, Ly6G lymphocyte antigen 6 complex locus G6D

Journal: Journal of Translational Medicine

Article Title: Bone morphogenetic protein 10 serves as a biomarker and a potential therapeutic target for endothelial dysfunction in endotoxin-induced acute lung injury

doi: 10.1186/s12967-025-06742-6

Figure Lengend Snippet: BMP10 ameliorates LPS-induced acute lung injury and inflammation. A H&E staining of lung sections demonstrated that BMP10 treatment mitigated LPS-induced thickening of the alveolar septal walls, reduced infiltration of inflammatory cells within the interstitium, and preserved the alveolar structure; Scale bar, 100 μm. B LPS-stimulated mice treated with BMP10 exhibited a significantly lower lung injury score compared with the LPS group ( *p < 0.05, n = 4 mice per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). C IF staining of BALF indicated that BMP10 treatment significantly decreased the recruitment of activated neutrophils into the alveolar space induced by LPS ( *p < 0.05, n = 4 mice per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test); Scale bar, 50 µm; Red, MPO; Green, Ly6G; Blue, DAPI; D The levels of proinflammatory cytokines, including TNFα and IL-6, in the BALF, blood, and pulmonary homogenate supernatants were significantly lower in BMP10-treated, LPS-stimulated mice compared with the LPS-stimulated mice group ( *p < 0.05, n = 3—5 mice per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). BMP10 bone morphogenetic protein 10, H&E hematoxylin and eosin, LPS lipopolysaccharide, IF immunofluorescence, BALF bronchoalveolar lavage fluid, TNF-α tumor necrosis factor alpha, MPO myeloperoxidase, Ly6G lymphocyte antigen 6 complex locus G6D

Article Snippet: After a 2-h interval, mice were treated with recombinant mouse BMP10 (6038-BP-025/CF, R&D system, Minneapolis, MN, USA) with a single dose of 1.0 μg i.p.

Techniques: Staining, Two Tailed Test, MANN-WHITNEY, Immunofluorescence

BMP10 mitigated LPS-induced increasing murine pulmonary endothelial permeability. A TEM of murine lung sections revealed that BMP10 treatment improved the LPS-induced disruption of pulmonary endothelial integrity and continuity, as well as reduced interstitial edema; Scale bar, 5 μm. B Quantitative IHC analysis of pulmonary VE-cadherin expression demonstrated that BMP10 treatment significantly inhibited the LPS-induced downregulation of VE-cadherin expression ( *p < 0.05, n = 3 mice per group); Scale bar, 100 μm; Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). C The total protein levels in the BALF were significantly lower in BMP10-treated, LPS-stimulated mice than in LPS-stimulated mice ( *p < 0.05, n = 4 mice per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). TEM transmission electron microscopy, BMP10 bone morphogenetic protein 10, LPS lipopolysaccharide, IHC immunohistochemistry, BALF bronchoalveolar lavage fluid, VE-cadherin vascular endothelial cadherin

Journal: Journal of Translational Medicine

Article Title: Bone morphogenetic protein 10 serves as a biomarker and a potential therapeutic target for endothelial dysfunction in endotoxin-induced acute lung injury

doi: 10.1186/s12967-025-06742-6

Figure Lengend Snippet: BMP10 mitigated LPS-induced increasing murine pulmonary endothelial permeability. A TEM of murine lung sections revealed that BMP10 treatment improved the LPS-induced disruption of pulmonary endothelial integrity and continuity, as well as reduced interstitial edema; Scale bar, 5 μm. B Quantitative IHC analysis of pulmonary VE-cadherin expression demonstrated that BMP10 treatment significantly inhibited the LPS-induced downregulation of VE-cadherin expression ( *p < 0.05, n = 3 mice per group); Scale bar, 100 μm; Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). C The total protein levels in the BALF were significantly lower in BMP10-treated, LPS-stimulated mice than in LPS-stimulated mice ( *p < 0.05, n = 4 mice per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). TEM transmission electron microscopy, BMP10 bone morphogenetic protein 10, LPS lipopolysaccharide, IHC immunohistochemistry, BALF bronchoalveolar lavage fluid, VE-cadherin vascular endothelial cadherin

Article Snippet: After a 2-h interval, mice were treated with recombinant mouse BMP10 (6038-BP-025/CF, R&D system, Minneapolis, MN, USA) with a single dose of 1.0 μg i.p.

Techniques: Permeability, Disruption, Expressing, Two Tailed Test, MANN-WHITNEY, Transmission Assay, Electron Microscopy, Immunohistochemistry

BMP10 inhibited LPS-induced murine pulmonary endothelial dysfunction and apoptosis. A Western blot analysis of murine lung homogenates revealed that VE-cadherin expression decreased, whereas the expression of angiopoietin-2, ICAM-1, and VCAM-1 increased following LPS stimulation. Treatment with BMP10 reversed these changes ( *p < 0.05, n = 4 mouse per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). B IF staining of murine lung sections indicated that BMP10 treatment prevented the LPS-induced downregulation of MCL-1 expression; Scale bars, 100 µm; Green, MCL-1; Blue, DAPI. C TUNEL staining of murine lung sections demonstrated that BMP10 treatment effectively inhibited LPS-induced pulmonary apoptosis; Scale bar, 50 µm. BMP10 bone morphogenetic protein 10, IF immunofluorescence, VE-cadherin vascular endothelial cadherin, ICAM-1 intercellular adhesion molecule 1, VCAM-1 vascular cell adhesion protein 1, LPS lipopolysaccharide, MCL-1 myeloid cell leukemia sequence 1, BCL-2 B-cell leukemia/lymphoma type 2, TUNEL terminal deoxynucleotidyl transferase dUTP nick end labeling

Journal: Journal of Translational Medicine

Article Title: Bone morphogenetic protein 10 serves as a biomarker and a potential therapeutic target for endothelial dysfunction in endotoxin-induced acute lung injury

doi: 10.1186/s12967-025-06742-6

Figure Lengend Snippet: BMP10 inhibited LPS-induced murine pulmonary endothelial dysfunction and apoptosis. A Western blot analysis of murine lung homogenates revealed that VE-cadherin expression decreased, whereas the expression of angiopoietin-2, ICAM-1, and VCAM-1 increased following LPS stimulation. Treatment with BMP10 reversed these changes ( *p < 0.05, n = 4 mouse per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). B IF staining of murine lung sections indicated that BMP10 treatment prevented the LPS-induced downregulation of MCL-1 expression; Scale bars, 100 µm; Green, MCL-1; Blue, DAPI. C TUNEL staining of murine lung sections demonstrated that BMP10 treatment effectively inhibited LPS-induced pulmonary apoptosis; Scale bar, 50 µm. BMP10 bone morphogenetic protein 10, IF immunofluorescence, VE-cadherin vascular endothelial cadherin, ICAM-1 intercellular adhesion molecule 1, VCAM-1 vascular cell adhesion protein 1, LPS lipopolysaccharide, MCL-1 myeloid cell leukemia sequence 1, BCL-2 B-cell leukemia/lymphoma type 2, TUNEL terminal deoxynucleotidyl transferase dUTP nick end labeling

Article Snippet: After a 2-h interval, mice were treated with recombinant mouse BMP10 (6038-BP-025/CF, R&D system, Minneapolis, MN, USA) with a single dose of 1.0 μg i.p.

Techniques: Western Blot, Expressing, Two Tailed Test, MANN-WHITNEY, Staining, TUNEL Assay, Immunofluorescence, Sequencing

BMP10 alleviated LPS-induced endothelial dysfunction both in vitro and in vivo through the canonical signaling pathway. HPMECs were cultured with 100 ng/ml of BMP10 for 24 h, followed by exposure to 10 μg/ml of LPS for a predetermined duration based on the study design. A Western blot analysis showed that 24 h of LPS stimulation significantly increased the protein expression levels of ICAM-1 and VCAM-1 in HPMECs. However, these changes were reversed by BMP10 treatment ( *p < 0.05, n = 4 per group); Data are presented as mean ± standard error of the mean, and group comparisons were analyzed using a two-tailed non-parametric test (Mann–Whitney U test). B IF staining of HPMECs demonstrated that BMP10 prevented the LPS-induced reduction in the expression of VE-cadherin and pSmad1/5/8, a marker of the BMP10-activated canonical signaling pathway, following 2 h of LPS stimulation; scale bars, 100 µm; Green, VE-cadherin; Red, pSmad1/5/8; Blue, DAPI. C Western blot analysis of lung homogenates revealed that 24 h of LPS stimulation significantly increased pSmad1/5/8 protein levels, but BMP10 treatment reversed these effects ( *p < 0.05, n = 4 per group); Data are presented as mean ± standard error of the mean, and group comparisons were analyzed using a two-tailed non-parametric test (Mann–Whitney U test). D Western blot analysis of HPMECs showed that 6 h of LPS stimulation significantly increased pSmad1/5/8 protein expression, which was similarly reversed by BMP10 pretreatment ( *p < 0.05, n = 4 per group); Data are presented as mean ± standard error of the mean, and groups were analyzed using a two-tailed non-parametric test (Mann–Whitney U test). HPMEC human pulmonary microvascular endothelial cell, LPS lipopolysaccharide, BMP10 bone morphogenetic protein 10, ICAM-1 intercellular adhesion molecule 1, VCAM-1 vascular cell adhesion protein 1, VE-cadherin vascular endothelial cadherin, pSmad1/5/8 phosphorylated small mother against decapentaplegic 1/5/8

Journal: Journal of Translational Medicine

Article Title: Bone morphogenetic protein 10 serves as a biomarker and a potential therapeutic target for endothelial dysfunction in endotoxin-induced acute lung injury

doi: 10.1186/s12967-025-06742-6

Figure Lengend Snippet: BMP10 alleviated LPS-induced endothelial dysfunction both in vitro and in vivo through the canonical signaling pathway. HPMECs were cultured with 100 ng/ml of BMP10 for 24 h, followed by exposure to 10 μg/ml of LPS for a predetermined duration based on the study design. A Western blot analysis showed that 24 h of LPS stimulation significantly increased the protein expression levels of ICAM-1 and VCAM-1 in HPMECs. However, these changes were reversed by BMP10 treatment ( *p < 0.05, n = 4 per group); Data are presented as mean ± standard error of the mean, and group comparisons were analyzed using a two-tailed non-parametric test (Mann–Whitney U test). B IF staining of HPMECs demonstrated that BMP10 prevented the LPS-induced reduction in the expression of VE-cadherin and pSmad1/5/8, a marker of the BMP10-activated canonical signaling pathway, following 2 h of LPS stimulation; scale bars, 100 µm; Green, VE-cadherin; Red, pSmad1/5/8; Blue, DAPI. C Western blot analysis of lung homogenates revealed that 24 h of LPS stimulation significantly increased pSmad1/5/8 protein levels, but BMP10 treatment reversed these effects ( *p < 0.05, n = 4 per group); Data are presented as mean ± standard error of the mean, and group comparisons were analyzed using a two-tailed non-parametric test (Mann–Whitney U test). D Western blot analysis of HPMECs showed that 6 h of LPS stimulation significantly increased pSmad1/5/8 protein expression, which was similarly reversed by BMP10 pretreatment ( *p < 0.05, n = 4 per group); Data are presented as mean ± standard error of the mean, and groups were analyzed using a two-tailed non-parametric test (Mann–Whitney U test). HPMEC human pulmonary microvascular endothelial cell, LPS lipopolysaccharide, BMP10 bone morphogenetic protein 10, ICAM-1 intercellular adhesion molecule 1, VCAM-1 vascular cell adhesion protein 1, VE-cadherin vascular endothelial cadherin, pSmad1/5/8 phosphorylated small mother against decapentaplegic 1/5/8

Article Snippet: After a 2-h interval, mice were treated with recombinant mouse BMP10 (6038-BP-025/CF, R&D system, Minneapolis, MN, USA) with a single dose of 1.0 μg i.p.

Techniques: In Vitro, In Vivo, Cell Culture, Western Blot, Expressing, Two Tailed Test, MANN-WHITNEY, Staining, Marker

BMP10 inhibited LPS-induced in vitro human pulmonary endothelial apoptosis. A TUNEL staining showed that BMP10 treatment effectively suppressed apoptosis of HPMECs induced by 24 h of LPS stimulation; scale bars, 100 µm. B IF staining of HPMECs demonstrated that BMP10 treatment inhibited the downregulation of MCL-1 expression caused by 24 h of LPS incubation; scale bars, 100 µm; Green, MCL-1; Blue, DAPI. C Western blot analysis of HPMECs showed an elevation in cleaved caspase 3 protein levels after 6 h of LPS stimulation, and treatment with BMP10 effectively inhibited caspase 3 cleavage ( *p < 0.05, n = 4 mouse per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). TUNEL terminal deoxynucleotidyl transferase dUTP nick end labeling, BMP10 bone morphogenetic protein 10, LPS lipopolysaccharide, IF immunofluorescence, HPMEC human pulmonary microvascular endovascular cell, MCL-1 myeloid cell leukemia sequence 1

Journal: Journal of Translational Medicine

Article Title: Bone morphogenetic protein 10 serves as a biomarker and a potential therapeutic target for endothelial dysfunction in endotoxin-induced acute lung injury

doi: 10.1186/s12967-025-06742-6

Figure Lengend Snippet: BMP10 inhibited LPS-induced in vitro human pulmonary endothelial apoptosis. A TUNEL staining showed that BMP10 treatment effectively suppressed apoptosis of HPMECs induced by 24 h of LPS stimulation; scale bars, 100 µm. B IF staining of HPMECs demonstrated that BMP10 treatment inhibited the downregulation of MCL-1 expression caused by 24 h of LPS incubation; scale bars, 100 µm; Green, MCL-1; Blue, DAPI. C Western blot analysis of HPMECs showed an elevation in cleaved caspase 3 protein levels after 6 h of LPS stimulation, and treatment with BMP10 effectively inhibited caspase 3 cleavage ( *p < 0.05, n = 4 mouse per group); Data were presented as mean ± standard error of mean, and groups were analyzed by two-tailed non-parametric test (Mann–Whitney U test). TUNEL terminal deoxynucleotidyl transferase dUTP nick end labeling, BMP10 bone morphogenetic protein 10, LPS lipopolysaccharide, IF immunofluorescence, HPMEC human pulmonary microvascular endovascular cell, MCL-1 myeloid cell leukemia sequence 1

Article Snippet: After a 2-h interval, mice were treated with recombinant mouse BMP10 (6038-BP-025/CF, R&D system, Minneapolis, MN, USA) with a single dose of 1.0 μg i.p.

Techniques: In Vitro, TUNEL Assay, Staining, Expressing, Incubation, Western Blot, Two Tailed Test, MANN-WHITNEY, Immunofluorescence, Sequencing

BMP10 is a biomarker for predicting mortality in ICU patients diagnosed with pneumonia-related acute respiratory failure requiring invasive mechanical ventilation. A Plasma levels of BMP10 on the day of recruitment and B on day 2 after recruitment were significantly higher in patients who died in the hospital than in those who survived; Data were presented as medians with interquartile ranges (IQR) and groups were analyzed by Mann–Whitney U test; BMP10 bone morphogenetic protein 10

Journal: Journal of Translational Medicine

Article Title: Bone morphogenetic protein 10 serves as a biomarker and a potential therapeutic target for endothelial dysfunction in endotoxin-induced acute lung injury

doi: 10.1186/s12967-025-06742-6

Figure Lengend Snippet: BMP10 is a biomarker for predicting mortality in ICU patients diagnosed with pneumonia-related acute respiratory failure requiring invasive mechanical ventilation. A Plasma levels of BMP10 on the day of recruitment and B on day 2 after recruitment were significantly higher in patients who died in the hospital than in those who survived; Data were presented as medians with interquartile ranges (IQR) and groups were analyzed by Mann–Whitney U test; BMP10 bone morphogenetic protein 10

Article Snippet: After a 2-h interval, mice were treated with recombinant mouse BMP10 (6038-BP-025/CF, R&D system, Minneapolis, MN, USA) with a single dose of 1.0 μg i.p.

Techniques: Biomarker Discovery, Clinical Proteomics, MANN-WHITNEY

Up-regulated local BMP10 expression in the right atrium of precPH patients. ( A ) Quantification of the relative BMP10 mRNA expression in control ( n = 9) and precPH ( n = 5 CTEPH) RA tissues. ( B and C ) Quantification of total RA BMP10 fluorescent area and RA cardiomyocytes BMP10 intensity levels in control ( n = 6) and precPH ( n = 4 PAH) paraffin-embedded RA tissue sections stained against BMP10, respectively. Representative immunofluorescent stainings of BMP10, Ulex-rhodamine (Ulex, endothelium), and cardiac TroponinT (cTnT, myocardium) in the negative control sample for anti-rabbit Alexa488 and anti-mouse Alexa647 ( D ), in the control ( E ), and in the precPH ( F ) RA tissues at 60×-oil magnification. ( D’–F’ ) Alexa488 single-channel images from the stainings in ( D–F ). ( E ′′ and F′′ ) Zoom-in images from ( E′ and F′ ) to appreciate the sarcomeric pattern of the BMP10 staining in the cardiomyocytes and the homogeneous staining in the vessels. Scale bars = 50 μm. Brightness and contrast for the Alexa488 channel have not been modified. Normality of data was checked and transformed if needed, and statistical differences between precPH patients and controls were tested using an independent sample t -test.

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: Up-regulated local BMP10 expression in the right atrium of precPH patients. ( A ) Quantification of the relative BMP10 mRNA expression in control ( n = 9) and precPH ( n = 5 CTEPH) RA tissues. ( B and C ) Quantification of total RA BMP10 fluorescent area and RA cardiomyocytes BMP10 intensity levels in control ( n = 6) and precPH ( n = 4 PAH) paraffin-embedded RA tissue sections stained against BMP10, respectively. Representative immunofluorescent stainings of BMP10, Ulex-rhodamine (Ulex, endothelium), and cardiac TroponinT (cTnT, myocardium) in the negative control sample for anti-rabbit Alexa488 and anti-mouse Alexa647 ( D ), in the control ( E ), and in the precPH ( F ) RA tissues at 60×-oil magnification. ( D’–F’ ) Alexa488 single-channel images from the stainings in ( D–F ). ( E ′′ and F′′ ) Zoom-in images from ( E′ and F′ ) to appreciate the sarcomeric pattern of the BMP10 staining in the cardiomyocytes and the homogeneous staining in the vessels. Scale bars = 50 μm. Brightness and contrast for the Alexa488 channel have not been modified. Normality of data was checked and transformed if needed, and statistical differences between precPH patients and controls were tested using an independent sample t -test.

Article Snippet: Finally, we could not determine BMP10 activity directly using trap antibody against BMP10 (#MAB2926, R&D Systems), as described, because this antibody did not inhibit BMP10 transcriptional activity in our samples; therefore, we used the ALK1-Fc.

Techniques: Expressing, Control, Staining, Negative Control, Modification, Transformation Assay

Up-regulated local BMP10 activity in the right atrium of precPH patients. ( A ) Quantification of positive pSMAD1/5/8 nuclei in vascular and non-vascular cells within the RA tissues from precPH ( n = 4 PAH) and controls ( n = 5). ( B and C ) Representative immunofluorescent staining of positive pSMAD1/5/8 nuclei in vascular and non-vascular cells from control and precPH with rhodamine and Alexa488 single-channel images on the sides. ( D ) Quantification of positive ID3 nuclei in vascular and non-vascular cells within the RA tissues from precPH ( n = 4 PAH) and controls ( n = 5). ( E and F ) Representative immunofluorescent staining of positive ID3 nuclei in vascular and non-vascular cells from control and precPH with rhodamine and Alexa488 single-channel images on the sides. Arrowheads indicate positive pSMAD1/5/8 and ID3 nuclei. Zoom-in images are included within ( B , C , E , and F ). Nuclei were counterstained with Hoechst 33342 and vessels with Ulex-rhodamine ( B , C , E , and F ). Negative control images are shown in , . Scale bars = 50 μm. Vascular and non-vascular measurements are plotted with their own Y -axis on the left or right side, respectively. Normality of data was checked and transformed if needed, and statistical differences between precPH patients and controls were tested using a Wilcoxon rank-sum test (in A and D ).

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: Up-regulated local BMP10 activity in the right atrium of precPH patients. ( A ) Quantification of positive pSMAD1/5/8 nuclei in vascular and non-vascular cells within the RA tissues from precPH ( n = 4 PAH) and controls ( n = 5). ( B and C ) Representative immunofluorescent staining of positive pSMAD1/5/8 nuclei in vascular and non-vascular cells from control and precPH with rhodamine and Alexa488 single-channel images on the sides. ( D ) Quantification of positive ID3 nuclei in vascular and non-vascular cells within the RA tissues from precPH ( n = 4 PAH) and controls ( n = 5). ( E and F ) Representative immunofluorescent staining of positive ID3 nuclei in vascular and non-vascular cells from control and precPH with rhodamine and Alexa488 single-channel images on the sides. Arrowheads indicate positive pSMAD1/5/8 and ID3 nuclei. Zoom-in images are included within ( B , C , E , and F ). Nuclei were counterstained with Hoechst 33342 and vessels with Ulex-rhodamine ( B , C , E , and F ). Negative control images are shown in , . Scale bars = 50 μm. Vascular and non-vascular measurements are plotted with their own Y -axis on the left or right side, respectively. Normality of data was checked and transformed if needed, and statistical differences between precPH patients and controls were tested using a Wilcoxon rank-sum test (in A and D ).

Techniques: Activity Assay, Staining, Control, Negative Control, Transformation Assay

Higher BMP10 plasma levels in precPH patients compared with controls. ( A and B ) BMP10 protein circulating plasma levels in precPH patients ( n = 48) and subgroups ( n = 48: 22 iPAH, 14 hPAH, and 12 CTEPH), respectively, vs. controls ( n = 16). ( C and D ) BMP9 protein circulating plasma levels in precPH patients ( n = 45) and subgroups ( n = 45: 20 iPAH, 14 hPAH, and 11 CTEPH), respectively, vs. controls ( n = 16). ( E and F ) Correlation between BMP10 and BMP9 plasma levels in precPH patients ( n = 45) or subgroups ( n = 45: 20 iPAH, 14 hPAH, and 11 CTEPH), respectively, vs. controls ( n = 16). Logarithmic Y -axis is used in graphs ( A – D ). Data in ( A and B ) are y + 1 for logarithmic scale transformation. Normality of data was checked and transformed if needed. Statistical differences between precPH patients or precPH subgroups and controls were tested with an independent sample t -test or a one-way ANOVA, respectively. Associations were tested with univariate linear regression analysis.

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: Higher BMP10 plasma levels in precPH patients compared with controls. ( A and B ) BMP10 protein circulating plasma levels in precPH patients ( n = 48) and subgroups ( n = 48: 22 iPAH, 14 hPAH, and 12 CTEPH), respectively, vs. controls ( n = 16). ( C and D ) BMP9 protein circulating plasma levels in precPH patients ( n = 45) and subgroups ( n = 45: 20 iPAH, 14 hPAH, and 11 CTEPH), respectively, vs. controls ( n = 16). ( E and F ) Correlation between BMP10 and BMP9 plasma levels in precPH patients ( n = 45) or subgroups ( n = 45: 20 iPAH, 14 hPAH, and 11 CTEPH), respectively, vs. controls ( n = 16). Logarithmic Y -axis is used in graphs ( A – D ). Data in ( A and B ) are y + 1 for logarithmic scale transformation. Normality of data was checked and transformed if needed. Statistical differences between precPH patients or precPH subgroups and controls were tested with an independent sample t -test or a one-way ANOVA, respectively. Associations were tested with univariate linear regression analysis.

Techniques: Clinical Proteomics, Transformation Assay

BMP10 transcriptional activity in precPH patients and controls. ( A ) Schematic explanation of the BRE-LUC reporter assay to determine BMP transcriptional activity in venous serum. Specific trap antibodies targeting BMP9 or BMP9 and BMP10 are used to assess BMP10 activity. Created with BioRender.com. B ) Relative BMP transcriptional activity as a luciferase read-out from the HMEC-BRE-LUC, endothelial cells expressing a BMP-specific luciferase reporter, in control ( n = 15) and precPH subgroups ( n = 21 iPAH, n = 13 hPAH, and n = 11 CTEPH) after incubation with phosphate-buffered saline (PBS) (baseline), anti-BMP9, or ALK1-Fc (inhibition of BMP9 and BMP10). ( C ) BMP10 activity in controls and precPH subgroups has been calculated from the subtraction of anti-BMP9 and ALK1-Fc to total BMP activity. Normality of data was checked and transformed if needed. Statistical differences between precPH patients and controls, and between baseline conditions and trap antibodies, were tested with an independent sample t -test or a one-way ANOVA, after which pairwise t -testing with Bonferroni correction was applied, respectively.

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: BMP10 transcriptional activity in precPH patients and controls. ( A ) Schematic explanation of the BRE-LUC reporter assay to determine BMP transcriptional activity in venous serum. Specific trap antibodies targeting BMP9 or BMP9 and BMP10 are used to assess BMP10 activity. Created with BioRender.com. B ) Relative BMP transcriptional activity as a luciferase read-out from the HMEC-BRE-LUC, endothelial cells expressing a BMP-specific luciferase reporter, in control ( n = 15) and precPH subgroups ( n = 21 iPAH, n = 13 hPAH, and n = 11 CTEPH) after incubation with phosphate-buffered saline (PBS) (baseline), anti-BMP9, or ALK1-Fc (inhibition of BMP9 and BMP10). ( C ) BMP10 activity in controls and precPH subgroups has been calculated from the subtraction of anti-BMP9 and ALK1-Fc to total BMP activity. Normality of data was checked and transformed if needed. Statistical differences between precPH patients and controls, and between baseline conditions and trap antibodies, were tested with an independent sample t -test or a one-way ANOVA, after which pairwise t -testing with Bonferroni correction was applied, respectively.

Techniques: Activity Assay, Reporter Assay, Luciferase, Expressing, Control, Incubation, Saline, Inhibition, Transformation Assay

$Patients with more right atrial dilatation, reduced RV ejection fraction, and higher NT-proBNP have higher levels of circulation BMP10 activity. ( A and B ) BMP10 transcriptional activity in precPH patients with RA or RV dilation, respectively. ( C–E ) BMP10 transcriptional activity in precPH patients with high RAP, reduced RVEF, or high NT-proBNP, respectively. PrecPH patients were stratified according to RA volume (>79 mL/mm 2 for male patients or >69 mL/mm 2 for female patients), RV end-diastolic volume index (≥109 mL/mm 2 for males, and ≥97 mL/mm 2 for females), RAP (>14 mmHg), RVEF (<35%), and NT-proBNP levels (>1100 ng/L). Normality of data was checked and transformed if needed. Statistical differences between both groups were tested with an independent samples t -test.$

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: Patients with more right atrial dilatation, reduced RV ejection fraction, and higher NT-proBNP have higher levels of circulation BMP10 activity. ( A and B ) BMP10 transcriptional activity in precPH patients with RA or RV dilation, respectively. ( C–E ) BMP10 transcriptional activity in precPH patients with high RAP, reduced RVEF, or high NT-proBNP, respectively. PrecPH patients were stratified according to RA volume (>79 mL/mm 2 for male patients or >69 mL/mm 2 for female patients), RV end-diastolic volume index (≥109 mL/mm 2 for males, and ≥97 mL/mm 2 for females), RAP (>14 mmHg), RVEF (<35%), and NT-proBNP levels (>1100 ng/L). Normality of data was checked and transformed if needed. Statistical differences between both groups were tested with an independent samples t -test.

Techniques: Activity Assay, Transformation Assay

Effect of pressure unloading on BMP10 activity in precPH patients. ( A ) Serum relative BMP activity at baseline and post-PEA in CTEPH patients. Incubation with anti-BMP9 only blocked BMP9 activity, while ALK1-Fc blocked both BMP9 and BMP10 activities. ( B ) Calculated BMP10 transcriptional activity at baseline and post-PEA ( n = 13), respectively. BMP10 transcriptional activity is calculated by subtracting BMP activity values after incubation with the trap antibodies. Normality of data was checked and transformed if needed. Statistical differences between baseline conditions and trap antibodies, and between baseline and post-PEA, were tested with an independent sample t -test.

Journal: Cardiovascular Research

Article Title: Bone morphogenetic protein 10 is increased in pre-capillary pulmonary hypertension patients

doi: 10.1093/cvr/cvaf028

Figure Lengend Snippet: Effect of pressure unloading on BMP10 activity in precPH patients. ( A ) Serum relative BMP activity at baseline and post-PEA in CTEPH patients. Incubation with anti-BMP9 only blocked BMP9 activity, while ALK1-Fc blocked both BMP9 and BMP10 activities. ( B ) Calculated BMP10 transcriptional activity at baseline and post-PEA ( n = 13), respectively. BMP10 transcriptional activity is calculated by subtracting BMP activity values after incubation with the trap antibodies. Normality of data was checked and transformed if needed. Statistical differences between baseline conditions and trap antibodies, and between baseline and post-PEA, were tested with an independent sample t -test.

Techniques: Activity Assay, Incubation, Transformation Assay

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