Downregulation of SMAD4 protects HaCaT cells against UVB-induced damage and oxidative stress through the activation of EMT

IF 2.7 3区化学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Photochemical & Photobiological Sciences Pub Date : 2024-04-29 DOI:10.1007/s43630-024-00574-x

Xiangzhi Li, Yimeng Wang, Xian Wang, Yi Shen, Yawen Yuan, Qingquan He, Shuyi Mao, Cailian Wu, Meijuan Zhou

{"title":"Downregulation of SMAD4 protects HaCaT cells against UVB-induced damage and oxidative stress through the activation of EMT","authors":"Xiangzhi Li, Yimeng Wang, Xian Wang, Yi Shen, Yawen Yuan, Qingquan He, Shuyi Mao, Cailian Wu, Meijuan Zhou","doi":"10.1007/s43630-024-00574-x","DOIUrl":null,"url":null,"abstract":"<p>As a member of the SMAD family, SMAD4 plays a crucial role in several cellular biological processes. However, its function in UVB radiation-induced keratinocyte damage is not yet clarified. Our study aims to provide mechanistic insight for the development of future UVB protective therapies and therapeutics involving SMAD4. HaCaT cells were treated with UVB, and the dose dependence and time dependence of UVB were measured. The cell function of UVB-treated HaCaT cells and the activity of epithelial-mesenchymal transition (EMT) after overexpression or silencing of SMAD4 was observed by flow cytometry, quantitative reverse transcription PCR (qRT-PCR) and Western Blots (WB). We found that a significant decrease in SMAD4 was observed in HaCaT cells induced by UVB. Our data confirm SMAD4 as a direct downstream target of miR-664. The down-regulation of SMAD4 preserved the viability of the UVB-treated HaCaT cells by inhibiting autophagy or apoptosis. Furthermore, the silencing of SMAD4 activated the EMT process in UVB-treated HaCaT cells. Down-regulation of SMAD4 plays a protective role in UVB-treated HaCaT cells via the activation of EMT.</p><h3 data-test=\"abstract-sub-heading\">Graphical abstract</h3>","PeriodicalId":98,"journal":{"name":"Photochemical & Photobiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.7000,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Photochemical & Photobiological Sciences","FirstCategoryId":"92","ListUrlMain":"https://doi.org/10.1007/s43630-024-00574-x","RegionNum":3,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

As a member of the SMAD family, SMAD4 plays a crucial role in several cellular biological processes. However, its function in UVB radiation-induced keratinocyte damage is not yet clarified. Our study aims to provide mechanistic insight for the development of future UVB protective therapies and therapeutics involving SMAD4. HaCaT cells were treated with UVB, and the dose dependence and time dependence of UVB were measured. The cell function of UVB-treated HaCaT cells and the activity of epithelial-mesenchymal transition (EMT) after overexpression or silencing of SMAD4 was observed by flow cytometry, quantitative reverse transcription PCR (qRT-PCR) and Western Blots (WB). We found that a significant decrease in SMAD4 was observed in HaCaT cells induced by UVB. Our data confirm SMAD4 as a direct downstream target of miR-664. The down-regulation of SMAD4 preserved the viability of the UVB-treated HaCaT cells by inhibiting autophagy or apoptosis. Furthermore, the silencing of SMAD4 activated the EMT process in UVB-treated HaCaT cells. Down-regulation of SMAD4 plays a protective role in UVB-treated HaCaT cells via the activation of EMT.

Graphical abstract

Abstract Image

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

下调 SMAD4 可通过激活 EMT 保护 HaCaT 细胞免受 UVB 诱导的损伤和氧化应激的影响

作为 SMAD 家族的成员，SMAD4 在多个细胞生物过程中发挥着至关重要的作用。然而，它在紫外线诱导的角质细胞损伤中的功能尚未明确。我们的研究旨在为未来开发 UVB 防护疗法和涉及 SMAD4 的疗法提供机理上的见解。用 UVB 处理 HaCaT 细胞，并测量 UVB 的剂量依赖性和时间依赖性。通过流式细胞术、定量反转录 PCR（qRT-PCR）和 Western Blots（WB）观察了 UVB 处理的 HaCaT 细胞的细胞功能以及过表达或沉默 SMAD4 后上皮-间质转化（EMT）的活性。我们发现，在 UVB 诱导的 HaCaT 细胞中，SMAD4 明显减少。我们的数据证实 SMAD4 是 miR-664 的直接下游靶标。下调 SMAD4 可抑制自噬或细胞凋亡，从而保持经 UVB 处理的 HaCaT 细胞的活力。此外，沉默 SMAD4 激活了 UVB 处理的 HaCaT 细胞的 EMT 过程。下调SMAD4可通过激活EMT在UVB处理的HaCaT细胞中发挥保护作用。

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分钟内获得全文去求助

来源期刊