Ling Chen , Yiliang Yin , Jingyun Li , Qian Li , Zezhang Zhu , Jun Li
{"title":"在增生性瘢痕成纤维细胞中,LINC00525通过前馈调节TGF-β信号传导促进细胞增殖和胶原表达。","authors":"Ling Chen , Yiliang Yin , Jingyun Li , Qian Li , Zezhang Zhu , Jun Li","doi":"10.1016/j.burns.2024.107353","DOIUrl":null,"url":null,"abstract":"<div><div>The etiology of hypertrophic scar formation continues to elude researchers, despite advancements in the understanding of skin scarring. Several long non-coding RNAs (lncRNAs) have been implicated in the pathogenesis of hypertrophic scars, yet the role and molecular mechanisms of LINC00525 in this process remain unclear. This study demonstrates that LINC00525 enhances cell proliferation and collagen expression through knockdown and overexpression techniques. Further analysis, including nuclear and cytoplasmic localization studies, RNA pull-down assays, bioinformatics predictions, and PCR validation, reveals that LINC00525 interacts with miR-29a-5p. The downregulation of LINC00525 enhances the expression of miR-29a-5p and suppresses the TGF-β/Smad signaling pathway. Additionally, TGF-β1 induces the upregulation of LINC00525. Collectively, these findings indicate that LINC00525 operates through a feedforward mechanism to regulate TGF-β signaling in hypertrophic scar fibroblasts. This research offers novel insights for the prevention and treatment of scars.</div></div>","PeriodicalId":50717,"journal":{"name":"Burns","volume":"51 2","pages":"Article 107353"},"PeriodicalIF":3.2000,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"LINC00525 promotes cell proliferation and collagen expression through feedforward regulation of TGF-β signaling in hypertrophic scar fibroblasts\",\"authors\":\"Ling Chen , Yiliang Yin , Jingyun Li , Qian Li , Zezhang Zhu , Jun Li\",\"doi\":\"10.1016/j.burns.2024.107353\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>The etiology of hypertrophic scar formation continues to elude researchers, despite advancements in the understanding of skin scarring. Several long non-coding RNAs (lncRNAs) have been implicated in the pathogenesis of hypertrophic scars, yet the role and molecular mechanisms of LINC00525 in this process remain unclear. This study demonstrates that LINC00525 enhances cell proliferation and collagen expression through knockdown and overexpression techniques. Further analysis, including nuclear and cytoplasmic localization studies, RNA pull-down assays, bioinformatics predictions, and PCR validation, reveals that LINC00525 interacts with miR-29a-5p. The downregulation of LINC00525 enhances the expression of miR-29a-5p and suppresses the TGF-β/Smad signaling pathway. Additionally, TGF-β1 induces the upregulation of LINC00525. Collectively, these findings indicate that LINC00525 operates through a feedforward mechanism to regulate TGF-β signaling in hypertrophic scar fibroblasts. This research offers novel insights for the prevention and treatment of scars.</div></div>\",\"PeriodicalId\":50717,\"journal\":{\"name\":\"Burns\",\"volume\":\"51 2\",\"pages\":\"Article 107353\"},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2024-12-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Burns\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0305417924003930\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CRITICAL CARE MEDICINE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Burns","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0305417924003930","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CRITICAL CARE MEDICINE","Score":null,"Total":0}
LINC00525 promotes cell proliferation and collagen expression through feedforward regulation of TGF-β signaling in hypertrophic scar fibroblasts
The etiology of hypertrophic scar formation continues to elude researchers, despite advancements in the understanding of skin scarring. Several long non-coding RNAs (lncRNAs) have been implicated in the pathogenesis of hypertrophic scars, yet the role and molecular mechanisms of LINC00525 in this process remain unclear. This study demonstrates that LINC00525 enhances cell proliferation and collagen expression through knockdown and overexpression techniques. Further analysis, including nuclear and cytoplasmic localization studies, RNA pull-down assays, bioinformatics predictions, and PCR validation, reveals that LINC00525 interacts with miR-29a-5p. The downregulation of LINC00525 enhances the expression of miR-29a-5p and suppresses the TGF-β/Smad signaling pathway. Additionally, TGF-β1 induces the upregulation of LINC00525. Collectively, these findings indicate that LINC00525 operates through a feedforward mechanism to regulate TGF-β signaling in hypertrophic scar fibroblasts. This research offers novel insights for the prevention and treatment of scars.
期刊介绍:
Burns aims to foster the exchange of information among all engaged in preventing and treating the effects of burns. The journal focuses on clinical, scientific and social aspects of these injuries and covers the prevention of the injury, the epidemiology of such injuries and all aspects of treatment including development of new techniques and technologies and verification of existing ones. Regular features include clinical and scientific papers, state of the art reviews and descriptions of burn-care in practice.
Topics covered by Burns include: the effects of smoke on man and animals, their tissues and cells; the responses to and treatment of patients and animals with chemical injuries to the skin; the biological and clinical effects of cold injuries; surgical techniques which are, or may be relevant to the treatment of burned patients during the acute or reconstructive phase following injury; well controlled laboratory studies of the effectiveness of anti-microbial agents on infection and new materials on scarring and healing; inflammatory responses to injury, effectiveness of related agents and other compounds used to modify the physiological and cellular responses to the injury; experimental studies of burns and the outcome of burn wound healing; regenerative medicine concerning the skin.