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

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