阿司匹林触发的RvD1 (AT-RvD1)调节香烟烟雾提取物刺激支气管上皮细胞的上皮-间质转化

IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Aline Beatriz Mahler Pereira , Bethânia Alves Gontijo , Sarah Cristina Sato Vaz Tanaka , Fernanda Bernadelli de Vito , Hélio Moraes de Souza , Paulo Roberto da Silva , Alexandre de Paula Rogerio
{"title":"阿司匹林触发的RvD1 (AT-RvD1)调节香烟烟雾提取物刺激支气管上皮细胞的上皮-间质转化","authors":"Aline Beatriz Mahler Pereira ,&nbsp;Bethânia Alves Gontijo ,&nbsp;Sarah Cristina Sato Vaz Tanaka ,&nbsp;Fernanda Bernadelli de Vito ,&nbsp;Hélio Moraes de Souza ,&nbsp;Paulo Roberto da Silva ,&nbsp;Alexandre de Paula Rogerio","doi":"10.1016/j.prostaglandins.2025.106968","DOIUrl":null,"url":null,"abstract":"<div><div>The epithelial-mesenchymal transition (EMT) plays significant role in airway remodeling during chronic obstructive pulmonary disease (COPD) and lung cancer. Aspirin-triggered resolvin D1 (AT-RvD1) presents anti-inflammatory and pro-resolution effects, via lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2). In addition, AT-RvD1 prevented TGF-β1-induced EMT in lung cancer cells (A549 cells). Here, we extend these results and evaluated the role of AT-RvD1 in cigarette smoke extract (CSE)-induced EMT on bronchial epithelial cells (BEAS-2B). CSE decreased E-cadherin expression, an epithelial marker, and increased ROS and TGF-β1 productions, and expressions of mesenchymal markers (N-cadherin, vimentin, smad2/3 and slug). Furthermore, CSE induced an increase in the ALX/FPR2 receptor expression. AT-RvD1 restored the expression of E-cadherin and reduced the N-cadherin, Vimentin, smad2/3 and ALX/FPR2 expressions as well as ROS and TGF-β1 productions on CSE-stimulated cells. In conclusion, AT-RvD1 has the potential to control epithelial-mesenchymal transition induced by smoking in the normal lung epithelial cells.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"177 ","pages":"Article 106968"},"PeriodicalIF":2.5000,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Aspirin-triggered RvD1 (AT-RvD1) modulates epithelial-mesenchymal transition on bronchial epithelial cells stimulated with cigarette smoke extract\",\"authors\":\"Aline Beatriz Mahler Pereira ,&nbsp;Bethânia Alves Gontijo ,&nbsp;Sarah Cristina Sato Vaz Tanaka ,&nbsp;Fernanda Bernadelli de Vito ,&nbsp;Hélio Moraes de Souza ,&nbsp;Paulo Roberto da Silva ,&nbsp;Alexandre de Paula Rogerio\",\"doi\":\"10.1016/j.prostaglandins.2025.106968\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>The epithelial-mesenchymal transition (EMT) plays significant role in airway remodeling during chronic obstructive pulmonary disease (COPD) and lung cancer. Aspirin-triggered resolvin D1 (AT-RvD1) presents anti-inflammatory and pro-resolution effects, via lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2). In addition, AT-RvD1 prevented TGF-β1-induced EMT in lung cancer cells (A549 cells). Here, we extend these results and evaluated the role of AT-RvD1 in cigarette smoke extract (CSE)-induced EMT on bronchial epithelial cells (BEAS-2B). CSE decreased E-cadherin expression, an epithelial marker, and increased ROS and TGF-β1 productions, and expressions of mesenchymal markers (N-cadherin, vimentin, smad2/3 and slug). Furthermore, CSE induced an increase in the ALX/FPR2 receptor expression. AT-RvD1 restored the expression of E-cadherin and reduced the N-cadherin, Vimentin, smad2/3 and ALX/FPR2 expressions as well as ROS and TGF-β1 productions on CSE-stimulated cells. In conclusion, AT-RvD1 has the potential to control epithelial-mesenchymal transition induced by smoking in the normal lung epithelial cells.</div></div>\",\"PeriodicalId\":21161,\"journal\":{\"name\":\"Prostaglandins & other lipid mediators\",\"volume\":\"177 \",\"pages\":\"Article 106968\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2025-02-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Prostaglandins & other lipid mediators\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1098882325000218\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Prostaglandins & other lipid mediators","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1098882325000218","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

上皮-间质转化(EMT)在慢性阻塞性肺疾病(COPD)和肺癌患者气道重塑中起重要作用。阿司匹林触发的溶解蛋白D1 (AT-RvD1)通过脂素A4受体/甲酰基肽受体2 (ALX/FPR2)具有抗炎和促溶解作用。此外,AT-RvD1可阻止TGF-β1诱导的肺癌细胞(A549细胞)EMT。在这里,我们扩展了这些结果,并评估了AT-RvD1在香烟烟雾提取物(CSE)诱导的支气管上皮细胞(BEAS-2B)的EMT中的作用。CSE降低了上皮标志物E-cadherin的表达,增加了ROS和TGF-β1的产生以及间质标志物(N-cadherin、vimentin、smad2/3和slug)的表达。此外,CSE诱导ALX/FPR2受体表达增加。AT-RvD1恢复了cse刺激细胞E-cadherin的表达,降低了N-cadherin、Vimentin、smad2/3和ALX/FPR2的表达以及ROS和TGF-β1的产生。综上所述,AT-RvD1具有控制吸烟诱导的正常肺上皮细胞上皮-间质转化的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Aspirin-triggered RvD1 (AT-RvD1) modulates epithelial-mesenchymal transition on bronchial epithelial cells stimulated with cigarette smoke extract
The epithelial-mesenchymal transition (EMT) plays significant role in airway remodeling during chronic obstructive pulmonary disease (COPD) and lung cancer. Aspirin-triggered resolvin D1 (AT-RvD1) presents anti-inflammatory and pro-resolution effects, via lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2). In addition, AT-RvD1 prevented TGF-β1-induced EMT in lung cancer cells (A549 cells). Here, we extend these results and evaluated the role of AT-RvD1 in cigarette smoke extract (CSE)-induced EMT on bronchial epithelial cells (BEAS-2B). CSE decreased E-cadherin expression, an epithelial marker, and increased ROS and TGF-β1 productions, and expressions of mesenchymal markers (N-cadherin, vimentin, smad2/3 and slug). Furthermore, CSE induced an increase in the ALX/FPR2 receptor expression. AT-RvD1 restored the expression of E-cadherin and reduced the N-cadherin, Vimentin, smad2/3 and ALX/FPR2 expressions as well as ROS and TGF-β1 productions on CSE-stimulated cells. In conclusion, AT-RvD1 has the potential to control epithelial-mesenchymal transition induced by smoking in the normal lung epithelial cells.
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
Prostaglandins & other lipid mediators
Prostaglandins & other lipid mediators 生物-生化与分子生物学
CiteScore
5.80
自引率
3.40%
发文量
49
审稿时长
2 months
期刊介绍: Prostaglandins & Other Lipid Mediators is the original and foremost journal dealing with prostaglandins and related lipid mediator substances. It includes basic and clinical studies related to the pharmacology, physiology, pathology and biochemistry of lipid mediators. Prostaglandins & Other Lipid Mediators invites reports of original research, mini-reviews, reviews, and methods articles in the basic and clinical aspects of all areas of lipid mediator research: cell biology, developmental biology, genetics, molecular biology, chemistry, biochemistry, physiology, pharmacology, endocrinology, biology, the medical sciences, and epidemiology. Prostaglandins & Other Lipid Mediators also accepts proposals for special issue topics. The Editors will make every effort to advise authors of the decision on the submitted manuscript within 3-4 weeks of receipt.
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信