Endothelial Cell Calcium Signaling during Barrier Function and Inflammation

Prarthana J. Dalal, William A. Muller, David P. Sullivan*

*Corresponding author for this work

Research output: Contribution to journalReview article

2 Scopus citations

Abstract

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 transendothelial migration.

Original languageEnglish (US)
Pages (from-to)535-542
Number of pages8
JournalAmerican Journal of Pathology
Volume190
Issue number3
DOIs
StatePublished - Mar 2020

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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