Lysophosphatidic acid 2 alleviates deep vein thrombosis via protective endothelial barrier function.

IF 1.7 4区 医学 Q2 MEDICINE, GENERAL & INTERNAL
Open Medicine Pub Date : 2025-02-06 eCollection Date: 2025-01-01 DOI:10.1515/med-2024-1137
Ruifeng Bai, Xinyang Yue, Xuan Tian, Huiru Zhao, Ying Liu, Tian Li, Jun Wu
{"title":"Lysophosphatidic acid 2 alleviates deep vein thrombosis via protective endothelial barrier function.","authors":"Ruifeng Bai, Xinyang Yue, Xuan Tian, Huiru Zhao, Ying Liu, Tian Li, Jun Wu","doi":"10.1515/med-2024-1137","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The specific role of lysophosphatidic acid 2 (LPA<sub>2</sub>) in deep vein thrombosis (DVT) remains unclear.</p><p><strong>Methods: </strong>An inferior vena cava annulus retraction model of DVT was established in wild-type (WT) and global LPA<sub>2</sub> knockout (<i>Lpar2</i> <sup><i>-/-</i></sup> ) mice. We examined the incidence of DVT, wet weight of thrombus, length of thrombus, assessed endothelial permeability through Evans blue dye assay <i>in vivo,</i> cell viability, and endothelial cell (EC) permeability of mouse inferior vena cava ECs <i>in vitro.</i> Proteomics, histopathology, immunohistochemistry, and western blotting were employed to investigate the role of LPA<sub>2</sub> in DVT.</p><p><strong>Results: </strong><i>Lpar2</i> deficiency increased vascular endothelial permeability and promoted the progression of DVT. Histological examination revealed aggravated inflammation in the thrombus of <i>Lpar2</i> <sup>-/-</sup> DVT mice. <i>In vitro</i>, <i>Lpar2</i> <sup>-/-</sup> resulted in increased permeability of ECs. Proteomic results indicated that DVT after <i>Lpar2</i> <sup>-/-</sup> may be related to tight junction (TJ) protein. LPA<sub>2</sub> agonist, 2-[4-(1,3-dioxo-1<i>H</i>,3<i>H</i>-benzoisoquinolin-2-yl)butylsulfamoyl] benzoic acid, significantly reduced vascular endothelial permeability as well as increased expression of the vascular endothelial TJ protein zonula occludens-1.</p><p><strong>Conclusion: </strong>These data provide a novel mechanism of endothelial barrier protection of LPA<sub>2</sub> in DVT.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"20 1","pages":"20241137"},"PeriodicalIF":1.7000,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11806235/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Open Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1515/med-2024-1137","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0

Abstract

Background: The specific role of lysophosphatidic acid 2 (LPA2) in deep vein thrombosis (DVT) remains unclear.

Methods: An inferior vena cava annulus retraction model of DVT was established in wild-type (WT) and global LPA2 knockout (Lpar2 -/- ) mice. We examined the incidence of DVT, wet weight of thrombus, length of thrombus, assessed endothelial permeability through Evans blue dye assay in vivo, cell viability, and endothelial cell (EC) permeability of mouse inferior vena cava ECs in vitro. Proteomics, histopathology, immunohistochemistry, and western blotting were employed to investigate the role of LPA2 in DVT.

Results: Lpar2 deficiency increased vascular endothelial permeability and promoted the progression of DVT. Histological examination revealed aggravated inflammation in the thrombus of Lpar2 -/- DVT mice. In vitro, Lpar2 -/- resulted in increased permeability of ECs. Proteomic results indicated that DVT after Lpar2 -/- may be related to tight junction (TJ) protein. LPA2 agonist, 2-[4-(1,3-dioxo-1H,3H-benzoisoquinolin-2-yl)butylsulfamoyl] benzoic acid, significantly reduced vascular endothelial permeability as well as increased expression of the vascular endothelial TJ protein zonula occludens-1.

Conclusion: These data provide a novel mechanism of endothelial barrier protection of LPA2 in DVT.

求助全文
约1分钟内获得全文 求助全文
来源期刊
Open Medicine
Open Medicine Medicine-General Medicine
CiteScore
3.00
自引率
0.00%
发文量
153
审稿时长
20 weeks
期刊介绍: Open Medicine is an open access journal that provides users with free, instant, and continued access to all content worldwide. The primary goal of the journal has always been a focus on maintaining the high quality of its published content. Its mission is to facilitate the exchange of ideas between medical science researchers from different countries. Papers connected to all fields of medicine and public health are welcomed. Open Medicine accepts submissions of research articles, reviews, case reports, letters to editor and book reviews.
×
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