ArticleDevelopmental biology2011
The cytoplasmic domain of TGFβR3 through its interaction with the scaffolding protein, GIPC, directs epicardial cell behavior.
Article in Developmental biology, 2011. 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, 36 citations in OpenAlex.
- GIPC1 governed ferroptosis by regulating DECR1-modulating lipid homeostasis during dilated cardiomyopathy (DCM).Cell death and differentiation · 2026Article
- Exploring TGFBR3 in disease pathogenesis: Mechanisms, clinical implications, and pharmacological modulation.Journal of pharmaceutical analysis · 2026Review
- A novel GDF1 frameshift mutation in a young adult with right coronary artery hypoplasia and myocardial bridging: a case report.Frontiers in cardiovascular medicine · 2026Article
- Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025Review
- TGF-β signaling regulates differentiation of MSCs in bone metabolism: disputes among viewpoints.Stem cell research & therapy · 2024Review
- Congenital Coronary Blood Vessel Anomalies: Animal Models and the Integration of Developmental Mechanisms.Advances in experimental medicine and biology · 2024Article
- Role of the Epicardium in the Development of the Atrioventricular Valves and Its Relevance to the Pathogenesis of Myxomatous Valve Disease.Journal of cardiovascular development and disease · 2021Review
- Epicardial Contribution to the Developing and Injured Heart: Exploring the Cellular Composition of the Epicardium.Frontiers in cardiovascular medicine · 2021Review
- Article
- Epicardial TGFβ and BMP Signaling in Cardiac Regeneration: What Lesson Can We Learn from the Developing Heart?Biomolecules · 2020Review
- Independent Origin of XY and ZW Sex Determination Mechanisms in Mosquitofish Sister Species.Genetics · 2020Article
- Mesothelium and Malignant Mesothelioma.Journal of developmental biology · 2019Review
- MicroRNA let-7a regulates angiogenesis by targeting TGFBR3 mRNA.Journal of cellular and molecular medicine · 2019Article
- Hypoxia Supports Epicardial Cell Differentiation in Vascular Smooth Muscle Cells through the Activation of the TGFβ Pathway.Journal of cardiovascular development and disease · 2018Article
- Transforming Growth Factor-β Receptor III is a Potential Regulator of Ischemia-Induced Cardiomyocyte Apoptosis.Journal of the American Heart Association · 2017Article
- H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction.Oncotarget · 2016Article
- Common pathways regulate Type III TGFβ receptor-dependent cell invasion in epicardial and endocardial cells.Cellular signalling · 2016Article
- BMP2 rescues deficient cell migration in Tgfbr3(-/-) epicardial cells and requires Src kinase.Cell adhesion & migration · 2016Article
- Epicardial Epithelial-to-Mesenchymal Transition in Heart Development and Disease.Journal of clinical medicine · 2016Review
- Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The epicardium is a major contributor of the cells that are required for the formation of coronary vessels. Mice lacking both copies of the gene encoding the Type III Transforming Growth Factor β Receptor (TGFβR3) fail to form the coronary vasculature, but the molecular mechanism by which TGFβR3 signals coronary vessel formation is unknown. We used intact embryos and epicardial cells from E11.5 mouse embryos to reveal the mechanisms by which TGFβR3 signals and regulates epicardial cell behavior. Analysis of E13.5 embryos reveals a lower rate of epicardial cell proliferation and decreased epicardially derived cell invasion in Tgfbr3(-/-) hearts. Tgfbr3(-/-) epicardial cells in vitro show decreased proliferation and decreased invasion in response to TGFβ1 and TGFβ2. Unexpectedly, loss of TGFβR3 also decreases responsiveness to two other important regulators of epicardial cell behavior, FGF2 and HMW-HA. Restoring full length TGFβR3 in Tgfbr3(-/-) cells rescued deficits in invasion in vitro in response TGFβ1 and TGFβ2 as well as FGF2 and HMW-HA. Expression of TGFβR3 missing the 3 C-terminal amino acids that are required to interact with the scaffolding protein GIPC1 did not rescue any of the deficits. Overexpression of GIPC1 alone in Tgfbr3(-/-) cells did not rescue invasion whereas knockdown of GIPC1 in Tgfbr3(+/+) cells decreased invasion in response to TGFβ2, FGF2, and HMW-HA. We conclude that TGFβR3 interaction with GIPC1 is critical for regulating invasion and growth factor responsiveness in epicardial cells and that dysregulation of epicardial cell proliferation and invasion contributes to failed coronary vessel development in Tgfbr3(-/-) mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.