{"title":"miR-942-5p通过靶向TRIM37阻止脓毒症诱导的急性肺损伤","authors":"Qiang Lu, Dinggao Zhang, Hui liu, Hao Xu","doi":"10.1111/iep.12413","DOIUrl":null,"url":null,"abstract":"<p>MicroRNAs (miRNAs) have been demonstrated to play pivotal roles in the pathogenesis of sepsis-induced acute lung injury (ALI). In this work, we aimed to clarify the potential role and the underlying mechanism of miR-942-5p in a lipopolysaccharide (LPS)-induced A549 cell injury model. The cell injury was evaluated by CCK-8 assay, flow cytometry and enzyme-linked immunosorbent assay (ELISA). The expression levels of miR-942-5p and tripartite motif-containing protein 37 (TRIM37) were measured by real-time PCR and Western blot, and their association was then validated by bioinformatics, luciferase reporter assay and RNA pull-down assay. We found that the expression of miR-942-5p was decreased in LPS-treated A549 cells. Furthermore, LPS treatment suppressed A549 cell viability, promoted apoptosis and increased the levels of inflammatory cytokines. Conversely, overexpression of miR-942-5p increased cell viability, reduced apoptosis and alleviated inflammatory cytokine secretion in the presence of LPS. Moreover, miR-942-5p directly targeted TRIM37 by binding to the 3′-UTR of TRIM37 mRNA. Upregulation of TRIM37 effectively reversed the anti-apoptotic and anti-inflammatory effects of miR-942-5p in LPS-induced A549 cells. Our findings suggested that miR-942-5p protected against LPS-induced cell injury through inhibiting apoptosis and inflammation in A549 cells by negatively regulating TRIM37.</p>","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"102 4-5","pages":"192-199"},"PeriodicalIF":1.8000,"publicationDate":"2021-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"9","resultStr":"{\"title\":\"miR-942-5p prevents sepsis-induced acute lung injury via targeting TRIM37\",\"authors\":\"Qiang Lu, Dinggao Zhang, Hui liu, Hao Xu\",\"doi\":\"10.1111/iep.12413\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>MicroRNAs (miRNAs) have been demonstrated to play pivotal roles in the pathogenesis of sepsis-induced acute lung injury (ALI). In this work, we aimed to clarify the potential role and the underlying mechanism of miR-942-5p in a lipopolysaccharide (LPS)-induced A549 cell injury model. The cell injury was evaluated by CCK-8 assay, flow cytometry and enzyme-linked immunosorbent assay (ELISA). The expression levels of miR-942-5p and tripartite motif-containing protein 37 (TRIM37) were measured by real-time PCR and Western blot, and their association was then validated by bioinformatics, luciferase reporter assay and RNA pull-down assay. We found that the expression of miR-942-5p was decreased in LPS-treated A549 cells. Furthermore, LPS treatment suppressed A549 cell viability, promoted apoptosis and increased the levels of inflammatory cytokines. Conversely, overexpression of miR-942-5p increased cell viability, reduced apoptosis and alleviated inflammatory cytokine secretion in the presence of LPS. Moreover, miR-942-5p directly targeted TRIM37 by binding to the 3′-UTR of TRIM37 mRNA. Upregulation of TRIM37 effectively reversed the anti-apoptotic and anti-inflammatory effects of miR-942-5p in LPS-induced A549 cells. Our findings suggested that miR-942-5p protected against LPS-induced cell injury through inhibiting apoptosis and inflammation in A549 cells by negatively regulating TRIM37.</p>\",\"PeriodicalId\":14157,\"journal\":{\"name\":\"International Journal of Experimental Pathology\",\"volume\":\"102 4-5\",\"pages\":\"192-199\"},\"PeriodicalIF\":1.8000,\"publicationDate\":\"2021-10-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"9\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Experimental Pathology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/iep.12413\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"PATHOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Experimental Pathology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/iep.12413","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PATHOLOGY","Score":null,"Total":0}
miR-942-5p prevents sepsis-induced acute lung injury via targeting TRIM37
MicroRNAs (miRNAs) have been demonstrated to play pivotal roles in the pathogenesis of sepsis-induced acute lung injury (ALI). In this work, we aimed to clarify the potential role and the underlying mechanism of miR-942-5p in a lipopolysaccharide (LPS)-induced A549 cell injury model. The cell injury was evaluated by CCK-8 assay, flow cytometry and enzyme-linked immunosorbent assay (ELISA). The expression levels of miR-942-5p and tripartite motif-containing protein 37 (TRIM37) were measured by real-time PCR and Western blot, and their association was then validated by bioinformatics, luciferase reporter assay and RNA pull-down assay. We found that the expression of miR-942-5p was decreased in LPS-treated A549 cells. Furthermore, LPS treatment suppressed A549 cell viability, promoted apoptosis and increased the levels of inflammatory cytokines. Conversely, overexpression of miR-942-5p increased cell viability, reduced apoptosis and alleviated inflammatory cytokine secretion in the presence of LPS. Moreover, miR-942-5p directly targeted TRIM37 by binding to the 3′-UTR of TRIM37 mRNA. Upregulation of TRIM37 effectively reversed the anti-apoptotic and anti-inflammatory effects of miR-942-5p in LPS-induced A549 cells. Our findings suggested that miR-942-5p protected against LPS-induced cell injury through inhibiting apoptosis and inflammation in A549 cells by negatively regulating TRIM37.
期刊介绍:
Experimental Pathology encompasses the use of multidisciplinary scientific techniques to investigate the pathogenesis and progression of pathologic processes. The International Journal of Experimental Pathology - IJEP - publishes papers which afford new and imaginative insights into the basic mechanisms underlying human disease, including in vitro work, animal models, and clinical research.
Aiming to report on work that addresses the common theme of mechanism at a cellular and molecular level, IJEP publishes both original experimental investigations and review articles. Recent themes for review series have covered topics as diverse as "Viruses and Cancer", "Granulomatous Diseases", "Stem cells" and "Cardiovascular Pathology".