Lin He, Chan Zhu, Huicong Dou, Xueyuan Yu, Jing Jia, Maoguo Shu
{"title":"瘢痕疙瘩核心因子 CTRP3 的过表达能显著控制 TGF-β1 诱导的瘢痕疙瘩成纤维细胞的繁殖和迁移。","authors":"Lin He, Chan Zhu, Huicong Dou, Xueyuan Yu, Jing Jia, Maoguo Shu","doi":"10.1155/2023/9638322","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Keloid is a type of benign fibrous proliferative tumor characterized by excessive scarring. C1q/TNF-related protein 3 (CTRP3) has been proven to possess antifibrotic effect. Here, we explored the role of CTRP3 in keloid. In the current research, we examined the influence of CTRP3 on keloid fibroblasts (KFs) and investigated the potential molecular mechanism.</p><p><strong>Methods: </strong>KF tissue specimens and adjacent normal fibroblast (NF) tissues were collected cultured from 10 keloid participants. For the TGF-<i>β</i>1 stimulation group, KFs were processed with human recombinant TGF-<i>β</i>1. Cell transfection of pcDNA3.1-CTRP3 or pcDNA3.1 was performed. The siRNA of CTRP3 (si-CTRP3) or negative control siRNA (si-scramble) was transfected into KFs.</p><p><strong>Results: </strong>CTRP3 was downregulated in keloid tissues and KFs. CTRP3 overexpression significantly controlled TGF-<i>β</i>1-induced propagation and migration in KFs. Col I, <i>α</i>-SMA, and fibronectin mRNA and protein levels were enhanced by TGF-<i>β</i>1 stimulation, whereas they were inhibited by CTRP3 overexpression. In contrast, CTRP3 knockdown exhibited the opposite effect. In addition, CTRP3 attenuated TGF-<i>β</i> receptors TRI and TRII in TGF-<i>β</i>1-induced KFs. Furthermore, CTRP3 prevented TGF-<i>β</i>1-stimulated nuclear translocation of smad2 and smad3 and suppressed the expression levels of p-smad2 and p-smad3 in KFs.</p><p><strong>Conclusion: </strong>CTRP3 exerted an antifibrotic role through inhibiting proliferation, migration, and ECM accumulation of KFs via regulating TGF-<i>β</i>1/Smad signal path.</p>","PeriodicalId":11201,"journal":{"name":"Disease Markers","volume":"2023 ","pages":"9638322"},"PeriodicalIF":0.0000,"publicationDate":"2023-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10115533/pdf/","citationCount":"1","resultStr":"{\"title\":\"Keloid Core Factor CTRP3 Overexpression Significantly Controlled TGF-<i>β</i>1-Induced Propagation and Migration in Keloid Fibroblasts.\",\"authors\":\"Lin He, Chan Zhu, Huicong Dou, Xueyuan Yu, Jing Jia, Maoguo Shu\",\"doi\":\"10.1155/2023/9638322\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>Keloid is a type of benign fibrous proliferative tumor characterized by excessive scarring. C1q/TNF-related protein 3 (CTRP3) has been proven to possess antifibrotic effect. Here, we explored the role of CTRP3 in keloid. In the current research, we examined the influence of CTRP3 on keloid fibroblasts (KFs) and investigated the potential molecular mechanism.</p><p><strong>Methods: </strong>KF tissue specimens and adjacent normal fibroblast (NF) tissues were collected cultured from 10 keloid participants. For the TGF-<i>β</i>1 stimulation group, KFs were processed with human recombinant TGF-<i>β</i>1. Cell transfection of pcDNA3.1-CTRP3 or pcDNA3.1 was performed. The siRNA of CTRP3 (si-CTRP3) or negative control siRNA (si-scramble) was transfected into KFs.</p><p><strong>Results: </strong>CTRP3 was downregulated in keloid tissues and KFs. CTRP3 overexpression significantly controlled TGF-<i>β</i>1-induced propagation and migration in KFs. Col I, <i>α</i>-SMA, and fibronectin mRNA and protein levels were enhanced by TGF-<i>β</i>1 stimulation, whereas they were inhibited by CTRP3 overexpression. In contrast, CTRP3 knockdown exhibited the opposite effect. In addition, CTRP3 attenuated TGF-<i>β</i> receptors TRI and TRII in TGF-<i>β</i>1-induced KFs. Furthermore, CTRP3 prevented TGF-<i>β</i>1-stimulated nuclear translocation of smad2 and smad3 and suppressed the expression levels of p-smad2 and p-smad3 in KFs.</p><p><strong>Conclusion: </strong>CTRP3 exerted an antifibrotic role through inhibiting proliferation, migration, and ECM accumulation of KFs via regulating TGF-<i>β</i>1/Smad signal path.</p>\",\"PeriodicalId\":11201,\"journal\":{\"name\":\"Disease Markers\",\"volume\":\"2023 \",\"pages\":\"9638322\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-04-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10115533/pdf/\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Disease Markers\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1155/2023/9638322\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Disease Markers","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1155/2023/9638322","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
Keloid Core Factor CTRP3 Overexpression Significantly Controlled TGF-β1-Induced Propagation and Migration in Keloid Fibroblasts.
Purpose: Keloid is a type of benign fibrous proliferative tumor characterized by excessive scarring. C1q/TNF-related protein 3 (CTRP3) has been proven to possess antifibrotic effect. Here, we explored the role of CTRP3 in keloid. In the current research, we examined the influence of CTRP3 on keloid fibroblasts (KFs) and investigated the potential molecular mechanism.
Methods: KF tissue specimens and adjacent normal fibroblast (NF) tissues were collected cultured from 10 keloid participants. For the TGF-β1 stimulation group, KFs were processed with human recombinant TGF-β1. Cell transfection of pcDNA3.1-CTRP3 or pcDNA3.1 was performed. The siRNA of CTRP3 (si-CTRP3) or negative control siRNA (si-scramble) was transfected into KFs.
Results: CTRP3 was downregulated in keloid tissues and KFs. CTRP3 overexpression significantly controlled TGF-β1-induced propagation and migration in KFs. Col I, α-SMA, and fibronectin mRNA and protein levels were enhanced by TGF-β1 stimulation, whereas they were inhibited by CTRP3 overexpression. In contrast, CTRP3 knockdown exhibited the opposite effect. In addition, CTRP3 attenuated TGF-β receptors TRI and TRII in TGF-β1-induced KFs. Furthermore, CTRP3 prevented TGF-β1-stimulated nuclear translocation of smad2 and smad3 and suppressed the expression levels of p-smad2 and p-smad3 in KFs.
Conclusion: CTRP3 exerted an antifibrotic role through inhibiting proliferation, migration, and ECM accumulation of KFs via regulating TGF-β1/Smad signal path.
期刊介绍：
Disease Markers is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies related to the identification of disease markers, the elucidation of their role and mechanism, as well as their application in the prognosis, diagnosis and treatment of diseases.
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