期刊
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
卷 29, 期 10, 页码 1509-U254出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.109.187559
关键词
JAM-C; ischemia reperfusion injury; leukocyte transmigration; inflammation; adhesion molecules
资金
- The Wellcome Trust, UK
- The British Heart Foundation [081172/Z/06/Z, PG/03/123/16102]
- WHR foundation and Kidney Research UK [PDF4/2009]
- Swiss National Science Foundation [310000-122430, 310000-120184]
- Juvenile Diabetes Research Foundation International [1-2007-158]
- EU [FP-7 BETAIMAGE 222980]
- Novo Nordisk
- Swiss National Foundation [310000-112551]
- Avenir Program, Inserm
- Oncosuisse [OCS-01812-12-2005]
- Kidney Research UK [PDF4/2009] Funding Source: researchfish
Objective-Junctional adhesion molecule-C (JAM-C) is an adhesion molecule that has multiple roles in inflammation and vascular biology, but many aspects of its functions under pathological conditions are unknown. Here we investigated the role of JAM-C in leukocyte migration in response to ischemia reperfusion (I/R) injury. Methods and Results-Pretreatment of mice with soluble JAM-C (sJAM-C), used as a pharmacological blocker of JAM-C-mediated reactions, significantly suppressed leukocyte migration in models of kidney and cremaster muscle I/R injury (39 and 51% inhibition, respectively). Furthermore, in the cremaster muscle model (studied by intravital microscopy), both leukocyte adhesion and transmigration were suppressed in JAM-C-deficient mice (JAM-C-/-) and enhanced in mice overexpressing JAM-C in their endothelial cells (ECs). Analysis of JAM-C subcellular expression by immunoelectron microscopy indicated that in I/R-injured tissues, EC JAM-C was redistributed from cytoplasmic vesicles and EC junctional sites to nonjunctional plasma membranes, a response that may account for the role of JAM-C in both leukocyte adhesion and transmigration under conditions of I/R injury. Conclusions-The findings demonstrate a role for EC JAM-C in mediating leukocyte adhesion and transmigration in response to I/R injury and indicate the existence of a novel regulatory mechanism for redistribution and hence function of EC JAM-C in vivo. (Arterioscler Thromb Vasc Biol. 2009; 29: 1509-1515.)
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