cAMP signaling in leukocyte transendothelial migration

被引：78

作者：

Lorenowicz, Magdalena J. ^{[1
]}

Fernandez-Borja, Mar ^{[1
]}

Hordijk, Peter L. ^{[1
]}

机构：

[1] Univ Amsterdam, Acad Med Ctr, Sanquin Res & Landsteiner Lab, NL-1066 CX Amsterdam, Netherlands

来源：

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY | 2007年 / 27卷 / 05期

关键词：

Epac; PKA; migration; leukocytes; endothelial cells;

D O I：

10.1161/ATVBAHA.106.132282

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The migration of leukocytes across the vascular endothelium is crucial for immunosurveillance as well as for inflammatory responses. Uncontrolled leukocyte transendothelial migration results in pathologies such as asthma, rheumatoid arthritis, and atherosclerosis. The molecular mechanisms that regulate leukocyte transendothelial migration involve signaling downstream of intracellular messengers such as cAMP, calcium, phosphoinositol lipids, or reactive oxygen species. Among these, cAMP is particularly intriguing because it is generated in both leukocytes and endothelial cells and regulates leukocyte chemotaxis as well as endothelial barrier function. In addition, physiological stimuli that induce cAMP production generate both pro-and antiinflammatory signals, underscoring the complexity of cAMP-driven signaling. This review discusses our current knowledge of the control of leukocyte transendothelial migration by two main cAMP effectors: protein kinase A and the Rap exchange factor Epac (Exchange protein directly activated by cAMP).

引用

页码：1014 / 1022

页数：9

共 104 条

[1] Monocytes induce reversible focal changes in vascular endothelial cadherin complex during transendothelial migration under flow [J].