TY - JOUR
T1 - Endothelial Cell Calcium Signaling during Barrier Function and Inflammation
AU - Dalal, Prarthana J.
AU - Muller, William A.
AU - Sullivan, David P.
N1 - Funding Information:
Supported by NIH grants R01 HL046849 (W.A.M.), R01 HL064774 (W.A.M.), T32GM8152 (P.J.D.), and F30HL134202 (P.J.D.).
Publisher Copyright:
© 2020 American Society for Investigative Pathology
PY - 2020/3
Y1 - 2020/3
N2 - 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.
AB - 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.
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U2 - 10.1016/j.ajpath.2019.11.004
DO - 10.1016/j.ajpath.2019.11.004
M3 - Review article
C2 - 31866349
AN - SCOPUS:85080868429
SN - 0002-9440
VL - 190
SP - 535
EP - 542
JO - American Journal of Pathology
JF - American Journal of Pathology
IS - 3
ER -