MAGI1 localizes to mature focal adhesion and modulates endothelial cell adhesion, migration and angiogenesis.

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Cell Adhesion & Migration Pub Date : 2021-12-01 DOI:10.1080/19336918.2021.1911472

Begoña Alday-Parejo, Kedar Ghimire, Oriana Coquoz, Gioele W Albisetti, Luca Tamò, Jelena Zaric, Jimmy Stalin, Curzio Rüegg

{"title":"MAGI1 localizes to mature focal adhesion and modulates endothelial cell adhesion, migration and angiogenesis.","authors":"Begoña Alday-Parejo, Kedar Ghimire, Oriana Coquoz, Gioele W Albisetti, Luca Tamò, Jelena Zaric, Jimmy Stalin, Curzio Rüegg","doi":"10.1080/19336918.2021.1911472","DOIUrl":null,"url":null,"abstract":"MAGI1 is an intracellular adaptor protein that stabilizes cell junctions and regulates epithelial and endothelial integrity. Here, we report that that in endothelial cells MAGI1 colocalizes with paxillin, β3-integrin, talin 1, tensin 3 and α-4-actinin at mature focal adhesions and actin stress fibers, and regulates their dynamics. Downregulation of MAGI1 reduces focal adhesion formation and maturation, cell spreading, actin stress fiber formation and RhoA/Rac1 activation. MAGI1 silencing increases phosphorylation of paxillin at Y118, an indicator of focal adhesion turnover. MAGI1 promotes integrin-dependent endothelial cells adhesion to ECM, reduces invasion and tubulogenesisin vitro and suppresses angiogenesis in vivo. Our results identify MAGI1 as anovel component of focal adhesions, and regulator of focal adhesion dynamics, cell adhesion, invasion and angiogenesis.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"15 1","pages":"126-139"},"PeriodicalIF":3.3000,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2021.1911472","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Adhesion & Migration","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/19336918.2021.1911472","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 9

Abstract

MAGI1 is an intracellular adaptor protein that stabilizes cell junctions and regulates epithelial and endothelial integrity. Here, we report that that in endothelial cells MAGI1 colocalizes with paxillin, β3-integrin, talin 1, tensin 3 and α-4-actinin at mature focal adhesions and actin stress fibers, and regulates their dynamics. Downregulation of MAGI1 reduces focal adhesion formation and maturation, cell spreading, actin stress fiber formation and RhoA/Rac1 activation. MAGI1 silencing increases phosphorylation of paxillin at Y118, an indicator of focal adhesion turnover. MAGI1 promotes integrin-dependent endothelial cells adhesion to ECM, reduces invasion and tubulogenesisin vitro and suppresses angiogenesis in vivo. Our results identify MAGI1 as anovel component of focal adhesions, and regulator of focal adhesion dynamics, cell adhesion, invasion and angiogenesis.

Abstract Image

查看原文本刊更多论文

MAGI1定位于成熟的局灶黏附，调节内皮细胞的黏附、迁移和血管生成。

MAGI1是一种细胞内接头蛋白，稳定细胞连接并调节上皮和内皮的完整性。在内皮细胞中，MAGI1与paxillin、β3-整合素、talin 1、tensin 3和α-4-actin蛋白共定位于成熟的局灶粘连和肌动蛋白应力纤维，并调节其动态。MAGI1的下调减少了局灶粘连的形成和成熟、细胞扩散、肌动蛋白应激纤维的形成和RhoA/Rac1的激活。mage1的沉默增加了paxillin在Y118位点的磷酸化，这是局灶性粘连转换的一个指标。MAGI1促进整合素依赖性内皮细胞粘附于ECM，减少体外入侵和小管生成，抑制体内血管生成。我们的研究结果表明，MAGI1是局灶黏附的新成分，是局灶黏附动力学、细胞黏附、侵袭和血管生成的调节剂。

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

Cell Adhesion & Migration CELL BIOLOGY-

CiteScore

6.40

自引率

0.00%

发文量

审稿时长

53 weeks

期刊介绍： Cell Adhesion & Migration is a multi-disciplinary, peer reviewed open access journal that focuses on the biological or pathological implications of cell-cell and cell-microenvironment interactions. The main focus of this journal is fundamental science. The journal strives to serve a broad readership by regularly publishing review articles covering specific disciplines within the field, and by publishing focused issues that provide an overview on specific topics of interest within the field. Cell Adhesion & Migration publishes relevant and timely original research, as well as authoritative overviews, commentaries, and perspectives, providing context for the work presented in Cell Adhesion & Migration and for key results published elsewhere. Original research papers may cover all topics important in the field of cell-cell and cell-matrix interactions. Cell Adhesion & Migration also publishes articles related to cell biomechanics, biomaterial, and development of related imaging technologies.