Endothelial Cell Calcium Signaling during Barrier Function and Inflammation

被引：167

作者：

Dalal, Prarthana J. ^{[1
]}

Muller, William A. ^{[1
]}

Sullivan, David P. ^{[1
]}

机构：

[1] Northwestern Univ, Dept Pathol, Feinberg Sch Med, 303 E Chicago Ave,Ward Bldg,Room 3-140, Chicago, IL 60611 USA

来源：

AMERICAN JOURNAL OF PATHOLOGY | 2020年 / 190卷 / 03期

关键词：

THROMBIN-INDUCED INCREASE; REGULATES NEUTROPHIL MIGRATION; TRANSENDOTHELIAL MIGRATION; VASCULAR-PERMEABILITY; P-SELECTIN; CA2+ ENTRY; ACTIVATION; EXPRESSION; CALMODULIN; TRANSIENT;

D O I：

10.1016/j.ajpath.2019.11.004

中图分类号：

R36 [病理学];

学科分类号：

100104 ;

摘要：

Calcium is an essential second messenger in endothelial cells and plays a pivotal role in regulating a number of physiologic processes, including cell migration, angiogenesis, barrier function, and inflammation. An increase in intracellular Ca2+ concentration can trigger a number of diverse signaling pathways under both physiologic and pathologic conditions. In this review, we discuss how calcium signaling pathways in endothelial cells play an essential role in affecting barrier function and facilitating inflammation. Inflammatory mediators, such as thrombin and histamine, increase intracellular calcium levels. This calcium influx causes adherens junction disassembly and cytoskeletal rearrangements to facilitate endothelial cell retraction and increased permeability. During inflammation endothelial cell calcium entry and the calcium-related signaling events also help facilitate several leukocyte-endothelial cell interactions, such as leukocyte rolling, adhesion, and ultimately trans endothelial migration.

引用

页码：535 / 542

页数：8

共 55 条

[1] Apocalmodulin Itself Promotes Ion Channel Opening and Ca2+ Regulation [J].