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 Letters590(8) pp. 1222​-1233​.​ DOI: https://doi.org/10.1002/1873-3468.12158 

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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

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