Transforming growth factor‐β induces loss of epithelial character and smooth muscle cell differentiation in epicardial cells
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During embryogenesis, epicardial cells undergo epithelial–mesenchymal transformation (EMT), invade the myocardium, and differentiate into components of the coronary vasculature, including smooth muscle cells. We tested the hypothesis that transforming growth factor‐β (TGFβ) stimulates EMT and smooth muscle differentiation of epicardial cells. In epicardial explants, TGFβ1 and TGFβ2 induce loss of epithelial morphology, cytokeratin, and membrane‐associated Zonula Occludens‐1 and increase the smooth muscle markers calponin and caldesmon. Inhibition of activin receptor‐like kinase (ALK) 5 blocks these effects, whereas constitutively active (ca) ALK5 increases cell invasion by 42%. Overexpression of Smad 3 did not mimic the effects of caALK5. Inhibition of p160 rho kinase or p38 MAP kinase prevented the loss of epithelial morphology in response to TGFβ, whereas only inhibition of p160 rho kinase blocked TGFβ‐stimulated caldesmon expression. These data demonstrate that TGFβ stimulates loss of epithelial character and smooth muscle differentiation in epicardial cells by means of a mechanism that requires ALK5 and p160 rho kinase. Developmental Dynamics 235:82–93, 2006. © 2005 Wiley‐Liss, Inc.
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The processes underlying AV EpiMT remain poorly characterized, as few studies assessing EpiMT focus on chamber epicardium.
“However, the processes underlying AV EpiMT remain poorly characterized, as the few studies assessing EpiMT focus on chamber epicardium25–29.”
From Cell diversity and plasticity during atrioventricular heart valve EMTs (2023) · cites this paper as [29]
The Introduction (page unavailable) says that factors regulating epicardial EMT remain largely unidentified, supporting the claim that its processes were poorly characterized. The Experimental Procedures describe explants grown from chick hearts placed ventral side down, but do not explicitly identify the sampled cells as chamber rather than AV epicardium. The paper also does not establish that the few EpiMT studies focused on chamber epicardium. (LLM, conf=0.78)
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References 68 · Cited by 112
Research works printed but not linked: 1
- Bakin AV, Rinehart C, Tomlinson AK, Ar- teaga CL. 2002. p38 mitogen-activated TGF ACTIONS ON EPICARDIAL CELLS 91 10970177, 2006, 1, Downloaded from https://anatomypubs.onlinelibrary.wiley.com/doi/10.1002/dvdy.20629 by Readcube (Labtiva Inc.), Wiley Online Library on [07/11/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License protein kinase is required for TGFbeta- mediated fibroblastic transdifferentia- tion and cell migration. J Cell Sci 115: 3193-3206. · DOI
- Authors
- Compton, L. A., Potash, D. A., Mundell, N. A., & Barnett, J. V.
- Affiliations
- Vanderbilt University Medical Center (US)
- Corresponding author
- Barnett, Joey V.
- Venue
- Developmental Dynamics
- Publisher
- Wiley
- Published
- 2005-10-28
- Volume
- 235
- Issue
- 1
- Pages
- 82-93
- ISSN
- 1058-8388 (ISSN-L)
- 1097-0177
- OpenAlex
- W2061415568
- Cited by
- 112
- References
- 68
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 5 · 2023: 2 · 2022: 4 · 2021: 4 · 2020: 4 · 2019: 4 · 2018: 6 · 2017: 1 · 2016: 5 · 2015: 2 · 2014: 5 · 2013: 7 · 2012: 10
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Developmental Dynamics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Vanderbilt University
- Vanderbilt-Ingram Cancer Center
- University of Toronto
- National Heart, Lung, and Blood Institute (HL 67105, R01HL052922, P01HL067105)
- National Institute of General Medical Sciences (T32GM007347)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- TGF-beta, epicardial cells, epithelial-mesenchymal transition, smooth muscle differentiation, ALK5, Rho kinase, p38 MAPK, caldesmon, calponin, ZO-1, cytokeratin, coronary vasculature development, myocardial invasion, Smad3
- MeSH terms
- Receptor, Transforming Growth Factor-beta Type I, Animals, Calmodulin-Binding Proteins, Cell Differentiation, Chick Embryo, Epithelium, Organ Culture Techniques, Pericardium, Transforming Growth Factor beta, Protein Serine-Threonine Kinases, Receptors, Transforming Growth Factor beta, Activin Receptors, Type I, Myocytes, Smooth Muscle, Intracellular Signaling Peptides and Proteins, p38 Mitogen-Activated Protein Kinases, rho-Associated Kinases
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