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Original Research Article | OPEN ACCESS

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

Yangrong Tan, Ling Liu, Shuiping Zhao, Wang Zhao

Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha, China;

For correspondence:-    

Accepted: 12 May 2022        Published: 30 June 2022

Citation: Tan Y, Liu L, Zhao S, Zhao W. Overexpression of TRPM7 suppresses AngII-induced phenotypic changes in hypertensive human vascular smooth muscle cells. Trop J Pharm Res 2022; 21(6):1221-1226 doi: 10.4314/tjpr.v21i6.13

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

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, α-SMA and OPN in AngII-induced HAVSMCs were determined, and the regulatory effects of TRPM7 on levels of α-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 α-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 α-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.

Keywords: Hypertension, Transient receptor potential cation channel subfamily M member 7 (TRPM7), Phenotype changes

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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