Shilin Tang, Yang Wang, Tanya Ma, Shijuan Lu, Kang Huang, Qiang Li, Miao Wu, Hui Yang, Jianghua Zhong
{"title":"MiR-30d 可抑制心肌细胞自噬，促进心肌梗死后的铁蛋白沉积。","authors":"Shilin Tang, Yang Wang, Tanya Ma, Shijuan Lu, Kang Huang, Qiang Li, Miao Wu, Hui Yang, Jianghua Zhong","doi":"10.23736/S0031-0808.20.03979-8","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":19851,"journal":{"name":"Panminerva medica","volume":" ","pages":"249-255"},"PeriodicalIF":4.3000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"MiR-30d inhibits cardiomyocytes autophagy promoting ferroptosis after myocardial infarction.\",\"authors\":\"Shilin Tang, Yang Wang, Tanya Ma, Shijuan Lu, Kang Huang, Qiang Li, Miao Wu, Hui Yang, Jianghua Zhong\",\"doi\":\"10.23736/S0031-0808.20.03979-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>\",\"PeriodicalId\":19851,\"journal\":{\"name\":\"Panminerva medica\",\"volume\":\" \",\"pages\":\"249-255\"},\"PeriodicalIF\":4.3000,\"publicationDate\":\"2024-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Panminerva medica\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.23736/S0031-0808.20.03979-8\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2020/7/27 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"0\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Panminerva medica","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.23736/S0031-0808.20.03979-8","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/7/27 0:00:00","PubModel":"Epub","JCR":"0","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
MiR-30d inhibits cardiomyocytes autophagy promoting ferroptosis after myocardial infarction.
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.
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).
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