m6A 'writer' KIAA1429 regulates the proliferation and migration of endothelial cells in atherosclerosis

Increasing evidences have illustrated the important role of N-6-methyladenosine (m(6)A) in atherosclerosis (AS). However, the role of m(6)A modification in AS pathophysiological process is still unknown. Here, the present work tried to investigate the expression and function of m(6)A methyltransferase KIAA1429 in AS pathology and explored its undergoing m(6)A-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 m(6)A 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 m(6)A/ROCK2 pathway. These findings provide new insights for m(6)A-mediated epigenetics in AS.