Decorin attenuates hypertrophic scar fibrosis via TGFβ/Smad signalling

IF 3.5 3区医学 Q1 DERMATOLOGY

Experimental Dermatology Pub Date : 2024-07-24 DOI:10.1111/exd.15133

Jiangtao Cui, Shiyi Zhang, Kiran Acharya, Yan Xu, Heng Guo, Tong Li, Donghe Fu, Zizhen Yang, Lingnan Hou, Xiaotao Xing, Xiaoyi Hu

{"title":"Decorin attenuates hypertrophic scar fibrosis via TGFβ/Smad signalling","authors":"Jiangtao Cui, Shiyi Zhang, Kiran Acharya, Yan Xu, Heng Guo, Tong Li, Donghe Fu, Zizhen Yang, Lingnan Hou, Xiaotao Xing, Xiaoyi Hu","doi":"10.1111/exd.15133","DOIUrl":null,"url":null,"abstract":"<p>The management of hypertrophic scars (HSs), characterized by excessive collagen production, involves various nonsurgical and surgical interventions. However, the absence of a well-defined molecular mechanism governing hypertrophic scarring has led to less-than-ideal results in clinical antifibrotic treatments. Therefore, our study focused on the role of decorin (DCN) and its regulatory role in the TGF-β/Smad signalling pathway in the development of HSs. In our research, we observed a decrease in DCN expression within hypertrophic scar tissue and its derived cells (HSFc) compared to that in normal tissue. Then, the inhibitory effect of DCN on collagen synthesis was confirmed in Fc and HSFc via the detection of fibrosis markers such as COL-1 and COL-3 after the overexpression and knockdown of DCN. Moreover, functional assessments revealed that DCN suppresses the proliferation, migration and invasion of HSFc. We discovered that DCN significantly inhibits the TGF-β1/Smad3 pathway by suppressing TGF-β1 expression, as well as the formation and phosphorylation of Smad3. This finding suggested that DCN regulates the synthesis of collagen-based extracellular matrix and fibrosis through the TGF-β1/Smad3 pathway.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"33 7","pages":""},"PeriodicalIF":3.5000,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental Dermatology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/exd.15133","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"DERMATOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

The management of hypertrophic scars (HSs), characterized by excessive collagen production, involves various nonsurgical and surgical interventions. However, the absence of a well-defined molecular mechanism governing hypertrophic scarring has led to less-than-ideal results in clinical antifibrotic treatments. Therefore, our study focused on the role of decorin (DCN) and its regulatory role in the TGF-β/Smad signalling pathway in the development of HSs. In our research, we observed a decrease in DCN expression within hypertrophic scar tissue and its derived cells (HSFc) compared to that in normal tissue. Then, the inhibitory effect of DCN on collagen synthesis was confirmed in Fc and HSFc via the detection of fibrosis markers such as COL-1 and COL-3 after the overexpression and knockdown of DCN. Moreover, functional assessments revealed that DCN suppresses the proliferation, migration and invasion of HSFc. We discovered that DCN significantly inhibits the TGF-β1/Smad3 pathway by suppressing TGF-β1 expression, as well as the formation and phosphorylation of Smad3. This finding suggested that DCN regulates the synthesis of collagen-based extracellular matrix and fibrosis through the TGF-β1/Smad3 pathway.

查看原文本刊更多论文

装饰素通过 TGFβ/Smad 信号减轻肥厚性疤痕纤维化。

增生性疤痕（HSs）的特点是胶原蛋白过度增生，其治疗涉及各种非手术和手术干预措施。然而，由于缺乏明确的分子机制来控制增生性疤痕，导致临床抗纤维化治疗的效果并不理想。因此，我们的研究重点放在了装饰素（DCN）的作用及其在TGF-β/Smad信号通路中对HS发展的调控作用上。在我们的研究中，我们观察到肥厚性瘢痕组织及其衍生细胞（HSFc）中 DCN 的表达比正常组织中的要低。然后，在过表达和敲除 DCN 后，通过检测纤维化标记物（如 COL-1 和 COL-3），证实了 DCN 在 Fc 和 HSFc 中对胶原合成的抑制作用。此外，功能评估显示 DCN 可抑制 HSFc 的增殖、迁移和侵袭。我们发现，DCN通过抑制TGF-β1的表达以及Smad3的形成和磷酸化，明显抑制了TGF-β1/Smad3通路。这一发现表明，DCN 通过 TGF-β1/Smad3 通路调节胶原细胞外基质的合成和纤维化。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Experimental Dermatology 医学-皮肤病学

CiteScore

6.70

自引率

5.60%

发文量

201

审稿时长

2 months

期刊介绍： Experimental Dermatology provides a vehicle for the rapid publication of innovative and definitive reports, letters to the editor and review articles covering all aspects of experimental dermatology. Preference is given to papers of immediate importance to other investigators, either by virtue of their new methodology, experimental data or new ideas. The essential criteria for publication are clarity, experimental soundness and novelty. Letters to the editor related to published reports may also be accepted, provided that they are short and scientifically relevant to the reports mentioned, in order to provide a continuing forum for discussion. Review articles represent a state-of-the-art overview and are invited by the editors.