Hypoxia-induced endothelial-mesenchymal transition is associated with RASAL1 promoter hypermethylation in human coronary endothelial cells
2016 | journal article. A publication with affiliation to the University of Göttingen.
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Hypoxia-induced endothelial-mesenchymal transition is associated with RASAL1 promoter hypermethylation in human coronary endothelial cells
Xu, X.; Tan, X.; Hulshoff, M. S.; Wilhelmi, T.; Zeisberg, M. & Zeisberg, E. M. (2016)
FEBS Letters, 590(8) pp. 1222-1233. DOI: https://doi.org/10.1002/1873-3468.12158
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Details
- Authors
- Xu, X.; Tan, Xiaoying; Hulshoff, Melanie S.; Wilhelmi, Tim; Zeisberg, Michael ; Zeisberg, Elisabeth M.
- Abstract
- Cardiac fibrosis is integral in chronic heart disease, and one of the cellular processes contributing to cardiac fibrosis is endothelial-to-mesenchymal transition (EndMT). We recently found that hypoxia efficiently induces human coronary artery endothelial cells (HCAEC) to undergo EndMT through a hypoxia inducible factor-1 alpha (HIF1 alpha)-dependent pathway. Promoter hypermethylation of Ras-Gap-like protein 1 (RASAL1) has also been recently associated with EndMT progression and cardiac fibrosis. Our findings suggest that HIF1 alpha and transforming growth factor (TGF)/SMAD signalling pathways synergistically regulate hypoxia-induced EndMT through both DNMT3a-mediated hypermethylation of RASAL1 promoter and direct SNAIL induction. The findings indicate that multiple cascades may be activated simultaneously to mediate hypoxia-induced EndMT.
- Issue Date
- 2016
- Status
- published
- Publisher
- Wiley
- Journal
- FEBS Letters
- ISSN
- 1873-3468