Ge-Ting Wu, Qiu-Yan Tian, Bin Xie, Yong-Bin Hu, Zheng-Hao Deng
{"title":"GDF15通过miR-338/STAT1激活矽肺中人成纤维细胞MRC5细胞。","authors":"Ge-Ting Wu, Qiu-Yan Tian, Bin Xie, Yong-Bin Hu, Zheng-Hao Deng","doi":"10.1007/s10238-025-01627-w","DOIUrl":null,"url":null,"abstract":"<p><p>Growth differentiation factor 15 (GDF-15) has been implicated in multiple biological functions. However, the role of GDF15 in silicosis remains unclear. In this study, the serum level of GDF-15 was investigated in 46 patients with silicosis by ELISA and results showed it was higher than that of control patients. The effects of exogenous GDF15 on mRNA and miRNA expression profiles of MRC5 cells were analyzed by RNA sequencing. GDF15 activated human embryonic lung fibroblast MRC5 cells with upregulation of col1a and α-SMA. GDF15 reduced miR-338 expression and increased STAT1 expression in MRC5 cells. The results of the luciferase reporter assay and bioinformatics analysis indicated that STAT1 was a direct target of miR-338. miR-338 mimics down-regulated col1a and α-SMA expression induced by GDF15 with STAT1 overexpression, whereas miR-338 inhibitor up-regulated col1a and α-SMA expression induced by GDF15 with STAT1 knockdown. Those results indicated GDF15 activated MRC5 cells through the miR-338/STAT1 pathway and GDF-15 may play an important role in silicosis.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"25 1","pages":"91"},"PeriodicalIF":3.2000,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11925976/pdf/","citationCount":"0","resultStr":"{\"title\":\"GDF15 activates human fibroblast MRC5 cells via miR-338/STAT1 in silicosis.\",\"authors\":\"Ge-Ting Wu, Qiu-Yan Tian, Bin Xie, Yong-Bin Hu, Zheng-Hao Deng\",\"doi\":\"10.1007/s10238-025-01627-w\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Growth differentiation factor 15 (GDF-15) has been implicated in multiple biological functions. However, the role of GDF15 in silicosis remains unclear. In this study, the serum level of GDF-15 was investigated in 46 patients with silicosis by ELISA and results showed it was higher than that of control patients. The effects of exogenous GDF15 on mRNA and miRNA expression profiles of MRC5 cells were analyzed by RNA sequencing. GDF15 activated human embryonic lung fibroblast MRC5 cells with upregulation of col1a and α-SMA. GDF15 reduced miR-338 expression and increased STAT1 expression in MRC5 cells. The results of the luciferase reporter assay and bioinformatics analysis indicated that STAT1 was a direct target of miR-338. miR-338 mimics down-regulated col1a and α-SMA expression induced by GDF15 with STAT1 overexpression, whereas miR-338 inhibitor up-regulated col1a and α-SMA expression induced by GDF15 with STAT1 knockdown. Those results indicated GDF15 activated MRC5 cells through the miR-338/STAT1 pathway and GDF-15 may play an important role in silicosis.</p>\",\"PeriodicalId\":10337,\"journal\":{\"name\":\"Clinical and Experimental Medicine\",\"volume\":\"25 1\",\"pages\":\"91\"},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2025-03-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11925976/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical and Experimental Medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s10238-025-01627-w\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical and Experimental Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10238-025-01627-w","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
GDF15 activates human fibroblast MRC5 cells via miR-338/STAT1 in silicosis.
Growth differentiation factor 15 (GDF-15) has been implicated in multiple biological functions. However, the role of GDF15 in silicosis remains unclear. In this study, the serum level of GDF-15 was investigated in 46 patients with silicosis by ELISA and results showed it was higher than that of control patients. The effects of exogenous GDF15 on mRNA and miRNA expression profiles of MRC5 cells were analyzed by RNA sequencing. GDF15 activated human embryonic lung fibroblast MRC5 cells with upregulation of col1a and α-SMA. GDF15 reduced miR-338 expression and increased STAT1 expression in MRC5 cells. The results of the luciferase reporter assay and bioinformatics analysis indicated that STAT1 was a direct target of miR-338. miR-338 mimics down-regulated col1a and α-SMA expression induced by GDF15 with STAT1 overexpression, whereas miR-338 inhibitor up-regulated col1a and α-SMA expression induced by GDF15 with STAT1 knockdown. Those results indicated GDF15 activated MRC5 cells through the miR-338/STAT1 pathway and GDF-15 may play an important role in silicosis.
期刊介绍：
Clinical and Experimental Medicine (CEM) is a multidisciplinary journal that aims to be a forum of scientific excellence and information exchange in relation to the basic and clinical features of the following fields: hematology, onco-hematology, oncology, virology, immunology, and rheumatology. The journal publishes reviews and editorials, experimental and preclinical studies, translational research, prospectively designed clinical trials, and epidemiological studies. Papers containing new clinical or experimental data that are likely to contribute to changes in clinical practice or the way in which a disease is thought about will be given priority due to their immediate importance. Case reports will be accepted on an exceptional basis only, and their submission is discouraged. The major criteria for publication are clarity, scientific soundness, and advances in knowledge. In compliance with the overwhelmingly prevailing request by the international scientific community, and with respect for eco-compatibility issues, CEM is now published exclusively online.
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