Overexpression of TRPM7 suppresses AngII-induced phenotypic changes in hypertensive human vascular smooth muscle cells

Purpose: To study the role of TRPM7 in suppressing AngII-induced phenotype changes in human vascular smooth muscle cells (HAVSMCs). Methods: Relative levels of TRPM7, alpha-SMA and OPN in AngII-induced HAVSMCs were determined, and the regulatory effects of TRPM7 on levels of alpha-SMA and OPN, wound healing effect, 5-ethynyl-2'deoxyuridine (EdU)-positive ratio, and viability in AngII-induced HAVSMCs were assessed. A total of 159 patients with essential hypertension attending The Second Xiangya Hospital, Central South University, Changsha, China, and 70 healthy controls were enrolled; after treatment with angiotensin receptor blocker (ARB), changes in SBP, DBP and plasma level of TRPM7 in hypertension patients were examined. Potential correlation between TRPM7 level with SBP and DBP was assessed. Results: TRPM7 and alpha-SMA were downregulated, while OPN was upregulated in AngII-induced HAVSMCs, but this trend was partially reversed by losartan treatment (p < 0.05). Overexpression of TRPM7 reversed the expression changes of alpha-SMA and OPN in AngII-induced HAVSMCs. In addition, the overexpression of TRPM7 significantly inhibited the enhanced migratory and proliferative capacities in AngII-induced HAVSMCs (p < 0.05). After ARB treatment, SBP, DBP and plasma TRPM7 were significantly reduced in hypertension patients, while TRPM7 level positively correlated with SBP and DBP in hypertensive patients. Conclusion: Overexpression of TRPM7 blocked AngII-induced phenotype changes in HAVSMCs under the pathological circumstance of hypertension.