ArticleAngiogenesis2020
Exacerbated inflammatory signaling underlies aberrant response to BMP9 in pulmonary arterial hypertension lung endothelial cells.
Article in Angiogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- IL-33 Drives Endothelial-to-Mesenchymal Transition in Pulmonary Hypertension.Hypertension (Dallas, Tex. : 1979) · 2026Article
- BMP9 Modulates IL-33 Signaling to Mitigate EndMT in Pulmonary Arterial Hypertension.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Disrupting BMP/TGF-β Signaling: Modulation of AQP1 and TGFB1 in Human Pulmonary Microvascular Endothelial Cells.Comprehensive Physiology · 2025Article
- BMP9 regulates the endothelial secretome to drive pulmonary hypertension.bioRxiv : the preprint server for biology · 2025Article
- The Association of Circulating Bone Morphogenetic Protein 9 and Arterial Stiffness in Hypertensive Patients.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- From basic scientific research to the development of new drugs for pulmonary arterial hypertension: insights from activin-targeting agents.Breathe (Sheffield, England) · 2025Review
- Therapeutic challenges and new therapeutic targets for combined capillary pulmonary hypertension: a review.Frontiers in medicine · 2025Review
- Mechanisms of lung endothelial cell injury and survival in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024Review
- Pulmonary Arterial Hypertension and TGF-β Superfamily Signaling: Focus on Sotatercept.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024Review
- Effects of Modulating BMP9, BMPR2, and AQP1 on BMP Signaling in Human Pulmonary Microvascular Endothelial Cells.International journal of molecular sciences · 2024Article
- Bone morphogenetic protein signalling in pulmonary arterial hypertension: revisiting the BMPRII connection.Biochemical Society transactions · 2024Review
- Endothelial Overexpression of TGF-β-Induced Protein Impairs Venous Thrombus Resolution: Possible Role in CTEPH.JACC. Basic to translational science · 2024Article
- Article
- Interleukin-6 and pulmonary hypertension: from physiopathology to therapy.Frontiers in immunology · 2023Review
- Obesity accelerates endothelial-to-mesenchymal transition in adipose tissues of mice and humans.Frontiers in cardiovascular medicine · 2023Article
- Molecular mechanisms of coronary microvascular endothelial dysfunction in diabetes mellitus: focus on mitochondrial quality surveillance.Angiogenesis · 2022Review
- Different cardiovascular and pulmonary phenotypes for single- and double-knock-out mice deficient in BMP9 and BMP10.Cardiovascular research · 2022Article
- Emerging roles of inflammation-mediated endothelial-mesenchymal transition in health and disease.Inflammation and regeneration · 2022Review
- Kawasaki disease: lncRNA Slco4a1 regulates the progression of human umbilical vein endothelial cells by targeting the miR-335-5p/POU5F1 axis.Translational pediatrics · 2022Article
- Melatonin Attenuates Ischemia/Reperfusion-Induced Oxidative Stress by Activating Mitochondrial Fusion in Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Imbalanced transforming growth factor beta (TGFβ) and bone morphogenetic protein (BMP) signaling are postulated to favor a pathological pulmonary endothelial cell (EC) phenotype in pulmonary arterial hypertension (PAH). BMP9 is shown to reinstate BMP receptor type-II (BMPR2) levels and thereby mitigate hemodynamic and vascular abnormalities in several animal models of pulmonary hypertension (PH). Yet, responses of the pulmonary endothelium of PAH patients to BMP9 are unknown. Therefore, we treated primary PAH patient-derived and healthy pulmonary ECs with BMP9 and observed that stimulation induces transient transcriptional signaling associated with the process of endothelial-to-mesenchymal transition (EndMT). However, solely PAH pulmonary ECs showed signs of a mesenchymal trans-differentiation characterized by a loss of VE-cadherin, induction of transgelin (SM22α), and reorganization of the cytoskeleton. In the PAH cells, a prolonged EndMT signaling was found accompanied by sustained elevation of pro-inflammatory, pro-hypoxic, and pro-apoptotic signaling. Herein we identified interleukin-6 (IL6)-dependent signaling to be the central mediator required for the BMP9-induced phenotypic change in PAH pulmonary ECs. Furthermore, we were able to target the BMP9-induced EndMT process by an IL6 capturing antibody that normalized autocrine IL6 levels, prevented mesenchymal transformation, and maintained a functional EC phenotype in PAH pulmonary ECs. In conclusion, our results show that the BMP9-induced aberrant EndMT in PAH pulmonary ECs is dependent on exacerbated pro-inflammatory signaling mediated through IL6.
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