{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhao Y"],"funding":["Guizhou Science and Technology Department","Guizhou Provincial Health and Family Planning Commission","National Natural Science Foundation of China"],"pagination":["913039"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9649646"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9"],"pubmed_abstract":["N6-methylatidine (m6A) is involved in post-transcriptional metabolism and a variety of pathological processes. However, little is known about the role of m6A in vascular proliferative diseases, particularly in vascular smooth muscle cells (VSMCs) phenotype switching-induced neointimal hyperplasia. In the current study, we discovered that methyltransferase like 3 (METTL3) is a critical candidate for catalyzing a global increase in m6A in response to carotid artery injury and various VSMCs phenotype switching. The inhibited neointimal hyperplasia was obtained after <i>in vivo</i> gene transfer to knock-down <i>Mettl3</i>. <i>In vitro</i> overexpression of <i>Mettl3</i> resulted in increased VSMC proliferation, migration, and reduced contractile gene expression with a global elevation of m6A "],"journal":["Frontiers in cardiovascular medicine"],"pubmed_title":["Methyltransferase like 3-mediated N6-methylatidin methylation inhibits vascular smooth muscle cells phenotype switching <i>via</i> promoting phosphatidylinositol 3-kinase mRNA decay."],"pmcid":["PMC9649646"],"funding_grant_id":["81960066","Qiankehe Foundation-ZK [2022] General 671","82160047","gzwjkj2020-1-063","gzwjkj2020-1-067","81760042","81760072"],"pubmed_authors":["Qiu Z","Li C","Long X","Shi B","Zhao R","Xia A","Bai Z","Shen Y","Zhao Y","Xiong W","Gu N"],"additional_accession":[]},"is_claimable":false,"name":"Methyltransferase like 3-mediated N6-methylatidin methylation inhibits vascular smooth muscle cells phenotype switching <i>via</i> promoting phosphatidylinositol 3-kinase mRNA decay.","description":"N6-methylatidine (m6A) is involved in post-transcriptional metabolism and a variety of pathological processes. However, little is known about the role of m6A in vascular proliferative diseases, particularly in vascular smooth muscle cells (VSMCs) phenotype switching-induced neointimal hyperplasia. In the current study, we discovered that methyltransferase like 3 (METTL3) is a critical candidate for catalyzing a global increase in m6A in response to carotid artery injury and various VSMCs phenotype switching. The inhibited neointimal hyperplasia was obtained after <i>in vivo</i> gene transfer to knock-down <i>Mettl3</i>. <i>In vitro</i> overexpression of <i>Mettl3</i> resulted in increased VSMC proliferation, migration, and reduced contractile gene expression with a global elevation of m6A ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2026-07-14T14:23:17.853Z","creation":"2024-11-05T21:58:39.38Z"},"accession":"S-EPMC9649646","cross_references":{"pubmed":["36386358"],"doi":["10.3389/fcvm.2022.913039"]}}