ALKBH5 Regulates SPHK1-Dependent Endothelial Cell Angiogenesis Following Ischemic Stress
Demethylase
DOI:
10.3389/fcvm.2021.817304
Publication Date:
2022-01-20T06:54:41Z
AUTHORS (8)
ABSTRACT
Endothelial cells dysfunction has been reported in many heart diseases including acute myocardial infarction, and atherosclerosis. The molecular mechanism for endothelial the is still not clearly understood. We aimed to study role of m6A RNA demethylase alkB homolog 5 (ALKBH5) ECs angiogenesis during ischemic injury.ECs were treated with insults (lipopolysaccharide 1% hypoxia) determine ALKBH5 angiogenesis. siRNA mediated gene silencing was used examining loss function. In this study, we report that levels are upregulated following ischemia associated maintaining ischemia-induced To decipher action, found required maintain eNOS phosphorylation SPHK1 protein levels. alone or stress significantly increased mRNA methylation. contrast, METTL3 (RNA methyltransferase) overexpression resulted reduced expression SPHK1.We helps maintenance via methylation downstream eNOS-AKT signaling.
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