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METTL3-dependent N <sup>6</sup> -methyladenosine RNA modification mediates the atherogenic inflammatory cascades in vascular endothelium

Chian‐Shiu Chien, Julie Yi-Shuan Li, Yueh Chien, Mong‐Lien Wang, Aliaksandr A. Yarmishyn, Ping‐Hsing Tsai, Chi‐Chang Juan, Phu Hung Nguyen, Hao‐Min Cheng, Teh‐Ia Huo, Shih-Hwa Chiou, Shu Chien

2021Proceedings of the National Academy of Sciences161 citationsDOIOpen Access PDF

Abstract

Significance Using in vitro and in vivo approaches, this report demonstrated the increased METTL3 expression and m 6 A hypermethylation in response to disturbed flow and oscillatory shear stress. METTL3 hypermethylates m 6 A sites at various downstream targets, up-regulates NLRP1 and down-regulates KLF4, and elicits atherogenic responses. Collectively, METTL3 and m 6 A hypermethylation epigenetically regulates the atherogenic gene expression and phenotypes in the initiation of atherosclerosis. Our data may enlighten the field of RNA epigenetics in the pathogenic mechanisms of heart diseases.

Topics & Concepts

EpigeneticsIn vivoCell biologyEndotheliumPhenotypeInflammationGene expressionKLF4In vitroRNABiologyChemistryCancer researchGeneImmunologyGeneticsInduced pluripotent stem cellEmbryonic stem cellRNA modifications and cancerCancer-related molecular mechanisms researchCancer-related gene regulation
METTL3-dependent N <sup>6</sup> -methyladenosine RNA modification mediates the atherogenic inflammatory cascades in vascular endothelium | Litcius