染料木素通过CTGF信号通路抑制瘢痕疙瘩的内吞和纤维形成

IF 3.3 3区 医学 Q2 GENETICS & HEREDITY Genes and Nutrition Pub Date : 2024-10-28 DOI:10.1186/s12263-024-00758-1
Chun-Te Lu, Jiunn-Liang Ko, Chu-Chyn Ou, Chih-Ting Hsu, Yu-Ping Hsiao, Sheau-Chung Tang
{"title":"染料木素通过CTGF信号通路抑制瘢痕疙瘩的内吞和纤维形成","authors":"Chun-Te Lu, Jiunn-Liang Ko, Chu-Chyn Ou, Chih-Ting Hsu, Yu-Ping Hsiao, Sheau-Chung Tang","doi":"10.1186/s12263-024-00758-1","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>This study aimed to evaluate soy isoflavones' effect and potential use-specifically genistein-in treating human keloid fibroblast cells (KFs) and in a keloid tissue culture model.</p><p><strong>Methods: </strong>To investigate the effects of genistein on keloid, a wound-healing assay was performed to detect cell migration. Flow cytometry was used to measure apoptosis. Western blotting and immunofluorescence staining were performed to detect the expression of target proteins. KF tissues were isolated, cultured, and divided into the control, silenced connective tissue growth factor (CTGF) proteins, and shNC (negative control) groups.</p><p><strong>Results: </strong>Genistein suppressed cell proliferation and migration, triggering the cell cycle at the G2/M phase and increasing the expression of p53 dose-dependent in keloids. Genistein inhibited the expression of COL1A1, FN, and CTGF mRNA and protein. Knockdown CTGF reduced the migrated ability in KFs. Genistein also abated TGF-β1-induced keloid fibrosis through the endocytosis model. Separated and cultured the keloid patient's tissues decreased the cell migration ability by genistein treatment and was time-dose dependent.</p><p><strong>Conclusions: </strong>This study indicated that genistein-induced p53 undergoes cell cycle arrest via the CTGF pathway-inhibited keloid cultured cells, and genistein suppressed the primary keloid cell migration, suggesting that our research provides a new strategy for developing drugs for treating keloids.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":null,"pages":null},"PeriodicalIF":3.3000,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520065/pdf/","citationCount":"0","resultStr":"{\"title\":\"Genistein inhibited endocytosis and fibrogenesis in keloid via CTGF signaling pathways.\",\"authors\":\"Chun-Te Lu, Jiunn-Liang Ko, Chu-Chyn Ou, Chih-Ting Hsu, Yu-Ping Hsiao, Sheau-Chung Tang\",\"doi\":\"10.1186/s12263-024-00758-1\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>This study aimed to evaluate soy isoflavones' effect and potential use-specifically genistein-in treating human keloid fibroblast cells (KFs) and in a keloid tissue culture model.</p><p><strong>Methods: </strong>To investigate the effects of genistein on keloid, a wound-healing assay was performed to detect cell migration. Flow cytometry was used to measure apoptosis. Western blotting and immunofluorescence staining were performed to detect the expression of target proteins. KF tissues were isolated, cultured, and divided into the control, silenced connective tissue growth factor (CTGF) proteins, and shNC (negative control) groups.</p><p><strong>Results: </strong>Genistein suppressed cell proliferation and migration, triggering the cell cycle at the G2/M phase and increasing the expression of p53 dose-dependent in keloids. Genistein inhibited the expression of COL1A1, FN, and CTGF mRNA and protein. Knockdown CTGF reduced the migrated ability in KFs. Genistein also abated TGF-β1-induced keloid fibrosis through the endocytosis model. Separated and cultured the keloid patient's tissues decreased the cell migration ability by genistein treatment and was time-dose dependent.</p><p><strong>Conclusions: </strong>This study indicated that genistein-induced p53 undergoes cell cycle arrest via the CTGF pathway-inhibited keloid cultured cells, and genistein suppressed the primary keloid cell migration, suggesting that our research provides a new strategy for developing drugs for treating keloids.</p>\",\"PeriodicalId\":55123,\"journal\":{\"name\":\"Genes and Nutrition\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.3000,\"publicationDate\":\"2024-10-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520065/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Genes and Nutrition\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s12263-024-00758-1\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Genes and Nutrition","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12263-024-00758-1","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
引用次数: 0

摘要

背景:本研究旨在评估大豆异黄酮(特别是染料木素)在治疗人类瘢痕疙瘩成纤维细胞(KFs)和瘢痕疙瘩组织培养模型中的作用和潜在用途:为了研究染料木苷对瘢痕疙瘩的影响,进行了伤口愈合试验以检测细胞迁移。流式细胞仪用于测量细胞凋亡。用 Western 印迹法和免疫荧光染色法检测目标蛋白的表达。分离、培养 KF 组织,并将其分为对照组、沉默结缔组织生长因子(CTGF)蛋白组和 shNC(阴性对照)组:结果:在瘢痕疙瘩中,染料木素抑制细胞增殖和迁移,引发细胞周期进入 G2/M 期,并增加 p53 的剂量依赖性表达。染料木素抑制了 COL1A1、FN 和 CTGF mRNA 和蛋白质的表达。敲除 CTGF 会降低瘢痕疙瘩的迁移能力。染料木素还能通过内吞模型减轻 TGF-β1 诱导的瘢痕疙瘩纤维化。分离和培养的瘢痕疙瘩患者组织经染料木素处理后,细胞迁移能力下降,且与时间剂量有关:这项研究表明,染料木素诱导的p53通过CTGF途径抑制瘢痕疙瘩培养细胞的细胞周期停滞,染料木素抑制了原发性瘢痕疙瘩细胞的迁移,这表明我们的研究为开发治疗瘢痕疙瘩的药物提供了一种新策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Genistein inhibited endocytosis and fibrogenesis in keloid via CTGF signaling pathways.

Background: This study aimed to evaluate soy isoflavones' effect and potential use-specifically genistein-in treating human keloid fibroblast cells (KFs) and in a keloid tissue culture model.

Methods: To investigate the effects of genistein on keloid, a wound-healing assay was performed to detect cell migration. Flow cytometry was used to measure apoptosis. Western blotting and immunofluorescence staining were performed to detect the expression of target proteins. KF tissues were isolated, cultured, and divided into the control, silenced connective tissue growth factor (CTGF) proteins, and shNC (negative control) groups.

Results: Genistein suppressed cell proliferation and migration, triggering the cell cycle at the G2/M phase and increasing the expression of p53 dose-dependent in keloids. Genistein inhibited the expression of COL1A1, FN, and CTGF mRNA and protein. Knockdown CTGF reduced the migrated ability in KFs. Genistein also abated TGF-β1-induced keloid fibrosis through the endocytosis model. Separated and cultured the keloid patient's tissues decreased the cell migration ability by genistein treatment and was time-dose dependent.

Conclusions: This study indicated that genistein-induced p53 undergoes cell cycle arrest via the CTGF pathway-inhibited keloid cultured cells, and genistein suppressed the primary keloid cell migration, suggesting that our research provides a new strategy for developing drugs for treating keloids.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Genes and Nutrition
Genes and Nutrition 生物-遗传学
CiteScore
6.60
自引率
0.00%
发文量
14
审稿时长
6-12 weeks
期刊介绍: This journal examines the relationship between genetics and nutrition, with the ultimate goal of improving human health. It publishes original research articles and review articles on preclinical research data coming largely from animal, cell culture and other experimental models as well as critical evaluations of human experimental data to help deliver products with medically proven use.
期刊最新文献
Genistein inhibited endocytosis and fibrogenesis in keloid via CTGF signaling pathways. Quercetin supplementation in metabolic syndrome: nutrigenetic interactions with the Zbtb16 gene variant in rodent models. Hypothetical proteins of chicken-isolated Limosilactobacillus reuteri subjected to in silico analyses induce IL-2 and IL-10. Visnagin alleviates rheumatoid arthritis via its potential inhibitory impact on malate dehydrogenase enzyme: in silico, in vitro, and in vivo studies. Effects of the oral administration of glycosaminoglycans with or without native type II collagen on the articular cartilage transcriptome in an osteoarthritic-induced rabbit model.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1