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Panminerva Medica 2020 Jul 27

DOI: 10.23736/S0031-0808.20.03979-8

Copyright © 2020 EDIZIONI MINERVA MEDICA

language: English

MiR-30d inhibits cardiomyocytes autophagy promoting ferroptosis after myocardial infarction

Shilin TANG, Yang WANG, Tianyi MA, Shijuan LU, Kang HUANG, Qiang LI, Miao WU, Hui YANG, Jianghua ZHONG

Department of Cardiology, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China


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BACKGROUND: To investigate the effect of microRNA-30d (miR-30d) on autophagy and reveal the mechanism of autophagy promoting ferroptosis in H9C2 cells.
METHODS: First, we detected miR-30d expression of myocardial tissue in the sham and myocardial infarction (MI) group, and then analyzed by biochemical analysis and luciferase Genetic experiments to confirm its downstream target gene of. After using Lentivirus-ATG5 (LV-sh-ATG5) to effectively inhibit autophagy, in order to further clarify the possible mechanism of autophagy leading to ferroptosis in H9C2 cells, we have tested the relevant indicators ferroptosis.
RESULTS: We first found that miR-30d expression was down-regulated in myocardial tissue after MI, while autophagy increased, and autophagy was reduced when miR-30d was overexpressed, and then analyzed by biochemical analysis and luciferase Genetic experiments confirmed that ATG5 was a downstream target gene of miR-30d. After using Lentivirus-ATG5 (LV-shATG5) to effectively inhibit autophagy and up-regulate the expression of FTH1 and GPX4 in H9C2 cells, reduce the content of MDA, increase the content of GSH, and increase the activity of GPX4, suggesting that autophagy after MI may promote ferroptosis in H9C2 cells.
CONCLUSIONS: The expression of miR-30d decreased in cardiomyocytes after MI and which can inhibit autophagy by binding to ATG5. Furthermore, autophagy after MI may promote ferroptosis.


KEY WORDS: MiR-30d, ATG5; Autophagy; Ferroptosis; Myocardial infarction (MI)

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