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Endothelial Cell Calcium Signaling during Barrier Function and Inflammation.
Dalal, Prarthana J; Muller, William A; Sullivan, David P.
Afiliación
  • Dalal PJ; Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
  • Muller WA; Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
  • Sullivan DP; Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois. Electronic address: d-sullivan@northwestern.edu.
Am J Pathol ; 190(3): 535-542, 2020 03.
Article en En | MEDLINE | ID: mdl-31866349
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.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Trombina / Señalización del Calcio / Células Endoteliales / Inflamación Límite: Humans Idioma: En Revista: Am J Pathol Año: 2020 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Trombina / Señalización del Calcio / Células Endoteliales / Inflamación Límite: Humans Idioma: En Revista: Am J Pathol Año: 2020 Tipo del documento: Article
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