Lu Rong, Huanzhou Xue, Jianwei Hao, Jianjun Liu, Hao Xu
{"title":"长非编码 RNA MEG3 沉默通过海绵化和封存 miR-23c 来减少 LIN28B 的表达，从而减轻高血糖诱导的间质细胞损伤。","authors":"Lu Rong, Huanzhou Xue, Jianwei Hao, Jianjun Liu, Hao Xu","doi":"10.23876/j.krcp.23.090","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Diabetic nephropathy (DN) is a common kidney disease in diabetic patients. Long non-coding RNA maternally expressed gene 3 (MEG3) and microRNA (miR)-23c are reported to be implicated in DN development. Nevertheless, it is unclear that the molecular mechanism between MEG3 and miR-23c in DN remains unclear.</p><p><strong>Methods: </strong>Human mesangial cells (HMCs) were treated with high glucose (HG) to simulate the DN status in vitro. Expression of MEG3 and miR-23c was measured. Effects of MEG3 silencing on HG-stimulated HMC injury were determined. The relationship between MEG3 and miR-23c was verified by the dual-luciferase reporter and RNA immunoprecipitation assays.</p><p><strong>Results: </strong>MEG3 was overexpressed in serums from DN patients and HG-stimulated HMCs. MEG3 knockdown weakened HG-stimulated HMC proliferation, extracellular matrix (ECM) accumulation, and inflammation. MEG3 regulated lin-28 homolog B (LIN28B) expression through adsorbing miR-23c. MiR-23c inhibitor reversed MEG3 knockdown-mediated effects on HG-stimulated HMC proliferation, ECM accumulation, and inflammation. LIN28B overexpression overturned miR-23c mimic-mediated effects on HG-stimulated HMC proliferation, ECM accumulation, and inflammation.</p><p><strong>Conclusion: </strong>MEG3 regulated HMC injury via regulation of the miR-23c/LIN28B axis in DN, which can help us better understand the mechanism of DN mediated by MEG3.</p>","PeriodicalId":17716,"journal":{"name":"Kidney Research and Clinical Practice","volume":null,"pages":null},"PeriodicalIF":2.9000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11467368/pdf/","citationCount":"0","resultStr":"{\"title\":\"Long non-coding RNA MEG3 silencing weakens high glucose-induced mesangial cell injury by decreasing LIN28B expression by sponging and sequestering miR-23c.\",\"authors\":\"Lu Rong, Huanzhou Xue, Jianwei Hao, Jianjun Liu, Hao Xu\",\"doi\":\"10.23876/j.krcp.23.090\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Diabetic nephropathy (DN) is a common kidney disease in diabetic patients. Long non-coding RNA maternally expressed gene 3 (MEG3) and microRNA (miR)-23c are reported to be implicated in DN development. Nevertheless, it is unclear that the molecular mechanism between MEG3 and miR-23c in DN remains unclear.</p><p><strong>Methods: </strong>Human mesangial cells (HMCs) were treated with high glucose (HG) to simulate the DN status in vitro. Expression of MEG3 and miR-23c was measured. Effects of MEG3 silencing on HG-stimulated HMC injury were determined. The relationship between MEG3 and miR-23c was verified by the dual-luciferase reporter and RNA immunoprecipitation assays.</p><p><strong>Results: </strong>MEG3 was overexpressed in serums from DN patients and HG-stimulated HMCs. MEG3 knockdown weakened HG-stimulated HMC proliferation, extracellular matrix (ECM) accumulation, and inflammation. MEG3 regulated lin-28 homolog B (LIN28B) expression through adsorbing miR-23c. MiR-23c inhibitor reversed MEG3 knockdown-mediated effects on HG-stimulated HMC proliferation, ECM accumulation, and inflammation. LIN28B overexpression overturned miR-23c mimic-mediated effects on HG-stimulated HMC proliferation, ECM accumulation, and inflammation.</p><p><strong>Conclusion: </strong>MEG3 regulated HMC injury via regulation of the miR-23c/LIN28B axis in DN, which can help us better understand the mechanism of DN mediated by MEG3.</p>\",\"PeriodicalId\":17716,\"journal\":{\"name\":\"Kidney Research and Clinical Practice\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2024-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11467368/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Kidney Research and Clinical Practice\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.23876/j.krcp.23.090\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/12/11 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"UROLOGY & NEPHROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Kidney Research and Clinical Practice","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.23876/j.krcp.23.090","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/12/11 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"UROLOGY & NEPHROLOGY","Score":null,"Total":0}
Long non-coding RNA MEG3 silencing weakens high glucose-induced mesangial cell injury by decreasing LIN28B expression by sponging and sequestering miR-23c.
Background: Diabetic nephropathy (DN) is a common kidney disease in diabetic patients. Long non-coding RNA maternally expressed gene 3 (MEG3) and microRNA (miR)-23c are reported to be implicated in DN development. Nevertheless, it is unclear that the molecular mechanism between MEG3 and miR-23c in DN remains unclear.
Methods: Human mesangial cells (HMCs) were treated with high glucose (HG) to simulate the DN status in vitro. Expression of MEG3 and miR-23c was measured. Effects of MEG3 silencing on HG-stimulated HMC injury were determined. The relationship between MEG3 and miR-23c was verified by the dual-luciferase reporter and RNA immunoprecipitation assays.
Results: MEG3 was overexpressed in serums from DN patients and HG-stimulated HMCs. MEG3 knockdown weakened HG-stimulated HMC proliferation, extracellular matrix (ECM) accumulation, and inflammation. MEG3 regulated lin-28 homolog B (LIN28B) expression through adsorbing miR-23c. MiR-23c inhibitor reversed MEG3 knockdown-mediated effects on HG-stimulated HMC proliferation, ECM accumulation, and inflammation. LIN28B overexpression overturned miR-23c mimic-mediated effects on HG-stimulated HMC proliferation, ECM accumulation, and inflammation.
Conclusion: MEG3 regulated HMC injury via regulation of the miR-23c/LIN28B axis in DN, which can help us better understand the mechanism of DN mediated by MEG3.
期刊介绍：
Kidney Research and Clinical Practice (formerly The Korean Journal of Nephrology; ISSN 1975-9460, launched in 1982), the official journal of the Korean Society of Nephrology, is an international, peer-reviewed journal published in English. Its ISO abbreviation is Kidney Res Clin Pract. To provide an efficient venue for dissemination of knowledge and discussion of topics related to basic renal science and clinical practice, the journal offers open access (free submission and free access) and considers articles on all aspects of clinical nephrology and hypertension as well as related molecular genetics, anatomy, pathology, physiology, pharmacology, and immunology. In particular, the journal focuses on translational renal research that helps bridging laboratory discovery with the diagnosis and treatment of human kidney disease. Topics covered include basic science with possible clinical applicability and papers on the pathophysiological basis of disease processes of the kidney. Original researches from areas of intervention nephrology or dialysis access are also welcomed. Major article types considered for publication include original research and reviews on current topics of interest. Accepted manuscripts are granted free online open-access immediately after publication, which permits its users to read, download, copy, distribute, print, search, or link to the full texts of its articles to facilitate access to a broad readership. Circulation number of print copies is 1,600.
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