The role of junctional adhesion molecules in vascular inflammation

被引:388
作者
Weber, Christian [1 ]
Fraemohs, Line
Dejana, Elisabetta
机构
[1] RWTH Univ Hosp, Inst Mol Cardiovasc Res, D-52074 Aachen, Germany
[2] Univ Milan, FIRC Inst Mol Oncol, I-20139 Milan, Italy
[3] Univ Milan, Dept Biomol & Biotechnol Sci, I-20139 Milan, Italy
关键词
D O I
10.1038/nri2096
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Junctional adhesion molecules (JAMs) of the immunoglobulin superfamily are important in the control of vascular permeability and leukocyte transmigration across endothelial-cell surfaces, by engaging in homophilic, heterophilic and lateral interactions. Through their localization on the endothelial-cell surface and expression by platelets, JAMs contribute to adhesive interactions with circulating leukocytes and platelets. Antibody-blocking studies and studies using genetically modified mice have implicated these functions of JAMs in the regulation of leukocyte recruitment to sites of inflammation and ischaemia-reperfusion injury, in growth-factor-mediated angiogenesis, atherogenesis and neointima formation. The comparison of different JAM-family members and animal models, however, shows that the picture remains rather complex. This Review summarizes recent progress and future directions in understanding the role of JAMs as 'gate keepers' in inflammation and vascular pathology.
引用
收藏
页码:467 / 477
页数:11
相关论文
共 81 条
[1]   Cloning of human junctional adhesion molecule 3 (JAM3) and its identification as the JAM2 counter-receptor [J].
Arrate, MP ;
Rodriguez, JM ;
Tran, TM ;
Brock, TA ;
Cunningham, SA .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (49) :45826-45832
[2]   Junctional adhesion molecule-C regulates the early influx of leukocytes into tissues during inflammation [J].
Aurrand-Lions, M ;
Lamagna, C ;
Dangerfield, JP ;
Wang, SJ ;
Herrera, P ;
Nourshargh, S ;
Imhof, BA .
JOURNAL OF IMMUNOLOGY, 2005, 174 (10) :6406-6415
[3]   Heterogeneity of endothelial junctions is reflected by differential expression and specific subcellular localization of the three JAM family members [J].
Aurrand-Lions, M ;
Johnson-Leger, C ;
Wong, C ;
Du Pasquier, L ;
Imhof, BA .
BLOOD, 2001, 98 (13) :3699-3707
[4]   JAM-2, a novel immunoglobulin superfamily molecule, expressed by endothelial and lymphatic cells [J].
Aurrand-Lions, M ;
Duncan, L ;
Ballestrem, C ;
Imhof, BA .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (04) :2733-2741
[5]   F11-receptor (F11R/JAM) mediates platelet adhesion to endothelial cells: Role in inflammatory thrombosis [J].
Babinska, A ;
Kedees, MH ;
Athar, H ;
Ahmed, T ;
Batuman, C ;
Ehrlich, YH ;
Hussain, MM ;
Kornecki, E .
THROMBOSIS AND HAEMOSTASIS, 2002, 88 (05) :843-850
[6]   The FII receptor (FIIR/JAM-A) in atherothrombosis: Overexpression of FIIR in atherosclerotic plaques [J].
Babinska, Anna ;
Azari, Bani M. ;
Salifu, Moro O. ;
Liu, Ruijie ;
Jiang, Xian-Cheng ;
Sobocka, Malgorzata B. ;
Boo, Dorothy ;
Al Khoury, George ;
Deitch, Jonathan S. ;
Marmur, Jonathan D. ;
Ehrlich, Yigal H. ;
Kornecki, Elizabeth .
THROMBOSIS AND HAEMOSTASIS, 2007, 97 (02) :272-281
[7]   Hemophilic interaction of junctional adhesion molecule [J].
Bazzoni, G ;
Martìnez-Estrada, OM ;
Mueller, F ;
Nelboeck, P ;
Schmid, G ;
Bartfai, T ;
Dejana, E ;
Brockhaus, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (40) :30970-30976
[8]   Endothelial tight junctions: permeable barriers of the vessel wall [J].
Bazzoni, G .
THROMBOSIS AND HAEMOSTASIS, 2006, 95 (01) :36-42
[9]   Interaction of junctional adhesion molecule with the tight junction components ZO-1, cingulin, and occludin [J].
Bazzoni, G ;
Martínez-Estrada, OM ;
Orsenigo, F ;
Cordenonsi, M ;
Citi, S ;
Dejana, E .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (27) :20520-20526
[10]   The JAM family of junctional adhesion molecules [J].
Bazzoni, G .
CURRENT OPINION IN CELL BIOLOGY, 2003, 15 (05) :525-530