TRPM7 interference vector repaires injury caused by hypoxia/reoxygenation in cardiomyocyte cell line H9C2

Basic & Clinical Medicine ›› 2020, Vol. 40 ›› Issue (2): 209-214.

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TRPM7 interference vector repaires injury caused by hypoxia/reoxygenation in cardiomyocyte cell line H9C2

YANG Jue-sheng¹, FAN Hu-xiong³, HU Shan², GAO Ri-feng³, LU Fei⁴, WANG Heng⁵, TANG Yan-hua^1*

1. Department of Cardiovascular Surgery;
2. Department of Anesthesiology, the Second Affiliated Hospital of Nanchang University;
3. Medical Department of Graduate School of Nanchang University;
4. Department of Interventional , the Second Affiliated Hospital of Nanchang University, Nanchang 330031;
5. Department of Cardiothoracic Surgery, Pingdingshan Second People's Hospital, Pingdingshan 467000, China

Received:2019-05-20 Revised:2019-06-26 Online:2020-02-05 Published:2020-02-05
Contact: ^*tyh8565@163.com

Abstract

Abstract: Objective To study the repair function and mechanism of TRPM7 interference vector in hypoxic myocardial cell line (H9C2). Methods The hypoxia/reoxygenation model of H9C2 cardiomyocytes was established and the TRPM7 interference expression vector was constructed to transfect H9C2 cells. The expression of HIF1-α and TRPM7 in H9C2 cells was detected by RT-qPCR and Western blot. [Ca²⁺]_i and apoptosis was determined by flow cytometry. Results When H9C2 cells were transfected with TRPM7 interference vector, the expression of HIF1-α TTRPM7, the [Ca²⁺]_i concentration and the apoptosis rate all decreased. Conclusions TRPM7 interference vector has significant repairing effect on hypoxia H9C2 cardiomyocytes, and the mechanism may be mediated PI3K/Akt pathway.

Key words: TRPM7 interference vector, [Ca²⁺]_i, cell apoptosis

CLC Number:

R602

YANG Jue-sheng, FAN Hu-xiong, HU Shan, GAO Ri-feng, LU Fei, WANG Heng, TANG Yan-hua. TRPM7 interference vector repaires injury caused by hypoxia/reoxygenation in cardiomyocyte cell line H9C2[J]. Basic & Clinical Medicine, 2020, 40(2): 209-214.

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TRPM7 interference vector repaires injury caused by hypoxia/reoxygenation in cardiomyocyte cell line H9C2

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