Abstract
Increasing evidences have illustrated the important role of N6-methyladenosine (m6A) in atherosclerosis (AS). However, the role of m6A modification in AS pathophysiological process is still unknown. Here, the present work tried to investigate the expression and function of m6A methyltransferase KIAA1429 in AS pathology and explored its undergoing m6A-dependent molecular mechanism. Results indicated that KIAA1429 remarkedly up-regulated in oxidative low-density lipoprotein (ox-LDL)-treated human umbilical vein endothelial cells (HUVECs). KIAA1429 over-expression inhibited the proliferation/migration in ox-LDL-treated HUVECs, while, KIAA1429 knockdown up-regulated the proliferation and migration. Mechanistically, via m6A modification sites binding, ROCK2 mRNA was post-transcriptionally upregulated by KIAA1429 in response to Actinomycin D. Collectively, our study demonstrated the regulation of KIAA1429 on ox-LDL-induced HUVECs via m6A/ROCK2 pathway. These findings provide new insights for m6A-mediated epigenetics in AS.