N-methyladenosine (mA) writer METTL3 accelerates the apoptosis of vascular endothelial cells in high glucose.

Recent studies have shown that N-methyladenosine (mA) methylation, one of the most prevalent epigenetic modifications, is involved in diabetes mellitus. However, whether mA regulates diabetic vascular endothelium injury is still elusive. Present research aimed to investigate the regulation and mechanism of mA on vascular endothelium injury. Upregulation of METTL3 was observed in the high glucose (HG)-induced human umbilical vein endothelial cells (HUVECs), following with the upregulation of mA methylation level. Functionally, METTL3 silencing repressed the apoptosis and recovered the proliferation of HUVECs disposed by HG. Moreover, HG exposure upregulated the expression of suppressor of cytokine signaling3 (SOCS3). Mechanistically, METTL3 targeted the mA site on SOCS3 mRNA, which positively regulated the mRNA stability of SOCS3. In conclusion, METTL3 silencing attenuated the HG-induced vascular endothelium cells injury via promoting SOCS3 stability. In conclusion, this research expands the understanding of mA on vasculopathy in diabetes mellitus and provides a potential strategy for the protection of vascular endothelial injury.