{"title":"tRF5-22-SerGCT-1 protects the heart against myocardial injury by targeting MSK1.","authors":"Fanji Meng, Hemanyun Bai, Kangling Ke, Lingyan Fang, Haitao Huang, Xiao Liang, Weiyan Li, Xiongwen Chen, Can Chen","doi":"10.1080/17501911.2025.2495544","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>This study aims to explore the expression profiles and potential functions of tsRNAs in MI.</p><p><strong>Methods: </strong>Using a mouse model of MI induced by coronary artery ligation, we used smallRNA array to obtain tsRNAs expression profiles. Reverse transcription quantitative polymerase chain reaction(RT-qPCR), Western Blot, tRF5-22-SerGCT-1 mimics and inhibitors, cell proliferation and apoptosis detection, luciferase reporter assay, and bioinformatics analysis were employed to screen differentially expressed tsRNAs and identify the functions of tsRNAs after MI.</p><p><strong>Results: </strong>A total of 175 significantly different tsRNAs (FC > 1.5, <i>p</i> < 0.05) were identified in MI mice, including 98 upregulated and 77 downregulated tsRNAs. Bioinformatics and target gene prediction revealed that two differentially expressed tsRNAs (5'tiRNA-34-GlnCTG-4, tRF5-22-SerGCT-1) may be involved in processes like autophagy and apoptosis, as well as in key signaling pathways such as MAPK and autophagy. Further investigation of tRF5-22-SerGCT-1 revealed that its overexpression or inhibition in vitro affected MSK1 levels and cardiomyocytes apoptosis following oxygen-glucose deprivation, providing a protective effect. Dual-luciferase assays confirmed that tRF5-22-SerGCT-1 targets MSK1.</p><p><strong>Conclusion: </strong>We found differentially expressed tsRNAs in MI. In addition, our research showed first that tRF5-22-SerGCT-1 might be involved in the MAPK pathways by targeting the MSK1, modulating apoptosis.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":"17 7","pages":"439-451"},"PeriodicalIF":3.0000,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12026222/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Epigenomics","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/17501911.2025.2495544","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/23 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
引用次数: 0
Abstract
Aim: This study aims to explore the expression profiles and potential functions of tsRNAs in MI.
Methods: Using a mouse model of MI induced by coronary artery ligation, we used smallRNA array to obtain tsRNAs expression profiles. Reverse transcription quantitative polymerase chain reaction(RT-qPCR), Western Blot, tRF5-22-SerGCT-1 mimics and inhibitors, cell proliferation and apoptosis detection, luciferase reporter assay, and bioinformatics analysis were employed to screen differentially expressed tsRNAs and identify the functions of tsRNAs after MI.
Results: A total of 175 significantly different tsRNAs (FC > 1.5, p < 0.05) were identified in MI mice, including 98 upregulated and 77 downregulated tsRNAs. Bioinformatics and target gene prediction revealed that two differentially expressed tsRNAs (5'tiRNA-34-GlnCTG-4, tRF5-22-SerGCT-1) may be involved in processes like autophagy and apoptosis, as well as in key signaling pathways such as MAPK and autophagy. Further investigation of tRF5-22-SerGCT-1 revealed that its overexpression or inhibition in vitro affected MSK1 levels and cardiomyocytes apoptosis following oxygen-glucose deprivation, providing a protective effect. Dual-luciferase assays confirmed that tRF5-22-SerGCT-1 targets MSK1.
Conclusion: We found differentially expressed tsRNAs in MI. In addition, our research showed first that tRF5-22-SerGCT-1 might be involved in the MAPK pathways by targeting the MSK1, modulating apoptosis.
期刊介绍:
Epigenomics provides the forum to address the rapidly progressing research developments in this ever-expanding field; to report on the major challenges ahead and critical advances that are propelling the science forward. The journal delivers this information in concise, at-a-glance article formats – invaluable to a time constrained community.
Substantial developments in our current knowledge and understanding of genomics and epigenetics are constantly being made, yet this field is still in its infancy. Epigenomics provides a critical overview of the latest and most significant advances as they unfold and explores their potential application in the clinical setting.