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

IF 4.3 4区医学 0 MEDICINE, GENERAL & INTERNAL Panminerva medica Pub Date : 2024-09-01 Epub Date: 2020-07-27 DOI:10.23736/S0031-0808.20.03979-8

Shilin Tang, Yang Wang, Tanya Ma, Shijuan Lu, Kang Huang, Qiang Li, Miao Wu, Hui Yang, Jianghua Zhong

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Abstract

Background: The aim of this study was 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 GSH peroxidase (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.

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MiR-30d 可抑制心肌细胞自噬，促进心肌梗死后的铁蛋白沉积。

背景：研究microRNA-30d（miR-30d）对H9C2细胞自噬的影响，并揭示自噬促进高铁血症的机制：目的：研究microRNA-30d（miR-30d）对H9C2细胞自噬的影响，并揭示自噬促进铁变态反应的机制：首先检测假性和心肌梗死（MI）组心肌组织中miR-30d的表达，然后通过生化分析和荧光素酶基因实验证实其下游靶基因的表达。在利用慢病毒-ATG5（LV-sh-ATG5）有效抑制自噬后，为了进一步阐明自噬导致H9C2细胞铁变态的可能机制，我们对铁变态的相关指标进行了检测：我们首先发现心肌梗死后心肌组织中miR-30d表达下调，而自噬增加，miR-30d过表达时自噬减少，然后通过生化分析和荧光素酶基因实验证实ATG5是miR-30d的下游靶基因。利用慢病毒-ATG5（LV-shATG5）有效抑制了H9C2细胞的自噬，上调了FTH1和GPX4的表达，降低了MDA的含量，增加了GSH的含量，提高了GPX4的活性，表明MI后的自噬可能促进了H9C2细胞的铁变态反应：结论：心肌梗死后，miR-30d在心肌细胞中的表达量减少，它能通过与ATG5结合抑制自噬。此外，心肌梗死后的自噬可能会促进高铁血症。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Panminerva medica 医学-医学：内科

CiteScore

5.00

自引率

2.30%

发文量

199

审稿时长

>12 weeks

期刊介绍： Panminerva Medica publishes scientific papers on internal medicine. Manuscripts may be submitted in the form of editorials, original articles, review articles, case reports, special articles, letters to the Editor and guidelines. The journal aims to provide its readers with papers of the highest quality and impact through a process of careful peer review and editorial work. Duties and responsibilities of all the subjects involved in the editorial process are summarized at Publication ethics. Manuscripts are expected to comply with the instructions to authors which conform to the Uniform Requirements for Manuscripts Submitted to Biomedical Editors by the International Committee of Medical Journal Editors (ICMJE).