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R&D Systems recombinant mouse bmp10

<t>BMP10</t> 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

Recombinant Mouse Bmp10, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 3 article reviews

recombinant mouse bmp10 - by Bioz Stars, 2026-09

93/100 stars

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1) Product Images from "Bone morphogenetic protein 10 serves as a biomarker and a potential therapeutic target for endothelial dysfunction in endotoxin-induced acute lung injury"

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

Journal: Journal of Translational Medicine

doi: 10.1186/s12967-025-06742-6

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

Figure Legend 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

Techniques Used: 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

Figure Legend 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

Techniques Used: 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

Figure Legend 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

Techniques Used: 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

Figure Legend 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

Techniques Used: 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

Figure Legend 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

Techniques Used: 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

Figure Legend 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

Techniques Used: Biomarker Discovery, Clinical Proteomics, MANN-WHITNEY

Recombinant:

Article Title: Bone morphogenetic protein 10 serves as a biomarker and a potential therapeutic target for endothelial dysfunction in endotoxin-induced acute lung injury
Article Snippet: In the model of E-ALI, male C57BL/6 mice aged 8–12 weeks were divided into four groups: Group 1 (n = 12) received 50 μl of PBS intratracheal instillation (i.t.) and 200 μl of PBS intraperitoneal injection (i.p.); Group 2 (n = 12) received LPS (5 mg/kg) in 50 μl of PBS i.t. and 200 μl of PBS i.p.; Group 3 (n = 12) received LPS (5 mg/kg) in 50 μl of PBS i.t. along with BMP10 (1.0 μg) in 200 μl of PBS i.p..; Group 4 (n = 12) received 50 μl of PBS i.t. along with BMP10 (1.0 μg) in 200 μl of PBS i.p. Mice were exposed to 5 mg/kg Escherichia coli 0111:B4 LPS (Sigma–Aldrich, St. Louis, MO) in 50 μl of PBS i.t., as previously established in our research [ – ], or 50 μl of PBS without LPS. .. 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. ..

Article Title: Single-cell analysis defines a pancreatic fibroblast lineage that supports anti-tumor immunity
Article Snippet: Recombinant mouse BMP7 , RnD Systems , 5666-BP-010. .. Recombinant mouse BMP10 , RnD Systems , 6038-BP-025. .. Recombinant mouse IL6 , PeproTech , 216-16.

Image Search Results

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

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

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

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

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

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

Fig. 8 BMP10, but not BMP9, suppresses the development of AVMs caused by ENG- deficiency. a–e CD31 and SMA immunofluorescence staining on retinas isolated from P7 control (PBS-treated Scl-CreER-negative Eng-iKO, a, n = 28 retinas), PBS-treated Scl-CreER;Eng-iKO (b, n = 16), BMP9-treated Scl-CreER;Eng- iKO (c, n = 8), BMP10-treated Scl-CreER;Eng-iKO (d, n = 8), and BMP9/BMP10-treated Scl-CreER;Eng-iKO (e, n = 10) mice. Arrows mark arterio- venous shunts. a artery, v vein. Scale bars, 500 μm. f Quantifi- cation of the number of AVMs. Data are mean ± SD. One-way ANOVA followed by Tukey’s post hoc test

Journal: Angiogenesis

Article Title: BMP10 functions independently from BMP9 for the development of a proper arteriovenous network.

doi: 10.1007/s10456-022-09859-0

Figure Lengend Snippet: Fig. 8 BMP10, but not BMP9, suppresses the development of AVMs caused by ENG- deficiency. a–e CD31 and SMA immunofluorescence staining on retinas isolated from P7 control (PBS-treated Scl-CreER-negative Eng-iKO, a, n = 28 retinas), PBS-treated Scl-CreER;Eng-iKO (b, n = 16), BMP9-treated Scl-CreER;Eng- iKO (c, n = 8), BMP10-treated Scl-CreER;Eng-iKO (d, n = 8), and BMP9/BMP10-treated Scl-CreER;Eng-iKO (e, n = 10) mice. Arrows mark arterio- venous shunts. a artery, v vein. Scale bars, 500 μm. f Quantifi- cation of the number of AVMs. Data are mean ± SD. One-way ANOVA followed by Tukey’s post hoc test

Article Snippet: Control PBS, 100 ng of mouse BMP9 protein (R&D systems, 5566-BP), or 100 ng of mouse BMP10 protein (R&D systems, 6038-BP) was injected intraperitoneally and daily on the opposite side of the milk spot until the sample collection.

Techniques: Immunofluorescence, Staining, Isolation, Control

Figure 5. Cell lines preferentially respond to different ligand combinations (A) Responses were measured for, from left to right, NMuMG cells, NMuMG cells with ACVR1 knockdown (KD), NMuMG cells with BMPR2 KD, NMuMG cells with ACVRL1 overexpression (OX), and mESCs, using ﬂow cytometry of an integrated ﬂuorescent protein reporter (STAR Methods: Addressing of cell lines). Each cell line was exposed to a double titration of BMP2 and BMP9, and responses were quantiﬁed by taking the mean of at least 3 replicates. For each cell line, fold change is calculated relative to the baseline ﬂuorescence with no added ligand and then normalized by the maximum value. Responses at select ligand words (red circles) are analyzed further in (B). (B) For select ligand words from (A), the responses of each cell line are shown. Error bars indicate SD of at least 3 repeats. Ligand words were chosen by ﬁxing a threshold of 0.5 (gray dashed line) and identifying those ligand combinations yielding unique on- and off-target activation patterns. (C) Data from (B) are summarized by showing the response of each cell type (columns) to each ligand word (rows), illustrating that distinct ligand words can activate different subsets of cell types. (D) Responses of NMuMG, NMuMG with ACVR1 KD, and NMuMG with BMPR2 KD to BMP9 and BMP10 are shown, as in (A). (E) As in (B), the responses of each cell type at selected ligand words are shown. (F) As in (C), the responses of each cell type (columns) to each ligand word (rows) conﬁrm that distinct ligand words preferentially activate distinct groups of cell types. See also Table S1.

Journal: Cell systems

Article Title: Ligand-receptor promiscuity enables cellular addressing.

doi: 10.1016/j.cels.2022.03.001

Figure Lengend Snippet: Figure 5. Cell lines preferentially respond to different ligand combinations (A) Responses were measured for, from left to right, NMuMG cells, NMuMG cells with ACVR1 knockdown (KD), NMuMG cells with BMPR2 KD, NMuMG cells with ACVRL1 overexpression (OX), and mESCs, using ﬂow cytometry of an integrated ﬂuorescent protein reporter (STAR Methods: Addressing of cell lines). Each cell line was exposed to a double titration of BMP2 and BMP9, and responses were quantiﬁed by taking the mean of at least 3 replicates. For each cell line, fold change is calculated relative to the baseline ﬂuorescence with no added ligand and then normalized by the maximum value. Responses at select ligand words (red circles) are analyzed further in (B). (B) For select ligand words from (A), the responses of each cell line are shown. Error bars indicate SD of at least 3 repeats. Ligand words were chosen by ﬁxing a threshold of 0.5 (gray dashed line) and identifying those ligand combinations yielding unique on- and off-target activation patterns. (C) Data from (B) are summarized by showing the response of each cell type (columns) to each ligand word (rows), illustrating that distinct ligand words can activate different subsets of cell types. (D) Responses of NMuMG, NMuMG with ACVR1 KD, and NMuMG with BMPR2 KD to BMP9 and BMP10 are shown, as in (A). (E) As in (B), the responses of each cell type at selected ligand words are shown. (F) As in (C), the responses of each cell type (columns) to each ligand word (rows) conﬁrm that distinct ligand words preferentially activate distinct groups of cell types. See also Table S1.

Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Chemicals, Peptides, and Recombinant Proteins BMP2 R&D Systems Cat# 355-BM BMP9 R&D Systems Cat# 5566-BP BMP10 R&D Systems Cat# 6038-BP Fetal Bovine Serum Clontech Cat# 631367 Fetal Bovine Serum, ES Cell Qualified Gibco Cat# 16141 Leukemia Inhibitory Factor MilliporeSigma Cat# ESG1107 Trypsin Gibco Cat# 25200 Accutase Gibco Cat# A11105 Deposited Data Optimization and simulation results This paper https://doi.org/10.22002/D1.1692 Experimental measurements of BMP responses in multiple cell lines This paper https://doi.org/10.22002/D1.1692 Experimental Models: Cell Lines NMuMG sensor line Klumpe et al., 2022 N/A NMuMG sensor line with ACVR1 knockdown Klumpe et al., 2022 N/A NMuMG sensor line with BMPR2 knockdown Klumpe et al., 2022 N/A NMuMG sensor line with ACVRL1 overexpression Klumpe et al., 2022 N/A mESC sensor line Antebi et al., 2017 N/A Software and Algorithms MATLAB MathWorks N/A Python Python Software Foundation N/A Equilibrium Toolkit (EQTK) (Python) Bois, 2020 https://github.com/justinbois/eqtk and https://doi.org/10.22002/D1.1430 PromiSys (Python) This paper https://github.com/christinasu/PromiSys and https://doi.org/10.22002/D1.20047 Simulation and analysis code (Python) This paper https://github.com/christinasu/PromiSys and https://doi.org/10.22002/D1.20047 EasyFlow (MATLAB) Antebi et al., 2017 https://github.com/AntebiLab/easyflow

Techniques: Knockdown, Over Expression, Cytometry, Titration, Activation Assay

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recombinant mouse bmp10 (R&D Systems)

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1) Product Images from "Bone morphogenetic protein 10 serves as a biomarker and a potential therapeutic target for endothelial dysfunction in endotoxin-induced acute lung injury"

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