Importance of junctional adhesion molecule-C for neointimal hyperplasia and monocyte recruitment in atherosclerosis-prone mice-brief report.
OBJECTIVE
Although junctional adhesion molecule (JAM)-C has been implicated in the control of inflammatory leukocyte recruitment, its role in neointima formation after arterial injury has not been elucidated.


RESULTS
In apolipoprotein E-deficient (Apoe(-/-)) mice fed an atherogenic diet, antibody blockade of JAM-C significantly reduced neointimal hyperplasia after wire injury of carotid arteries without altering medial area and decreased neointimal macrophage but not smooth muscle cell (SMC) content. An increased expression of JAM-C was detected in colocalization with luminal SMCs 1 day after injury and neointimal SMCs after 3 weeks. Blocking JAM-C inhibited monocytic cell arrest and leukocyte adhesion to carotid arteries perfused ex vivo and in vivo. Furthermore, monocyte adhesion to activated coronary artery SMCs under flow conditions in vitro was diminished by blocking JAM-C.


CONCLUSIONS
Our data provide the first evidence for a crucial role of JAM-C in accelerated lesion formation and leukocyte recruitment in atherosclerosis-prone mice.
Shagdarsuren
Erdenechimeg
E
Institut für Molekulare Herz-Kreislaufforschung, Universitätsklinikum der RWTH Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany.
Djalali-Talab
Yassin
Y
Aurrand-Lions
Michel
M
Bidzhekov
Kiril
K
Liehn
Elisa A
EA
Imhof
Beat A
BA
Weber
Christian
C
Zernecke
Alma
A
D000818:Animals; D050197:Atherosclerosis / Q000378:metabolism / Q000473:pathology*; D002339:Carotid Arteries / Q000378:metabolism / Q000473:pathology*; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D004195:Disease Models, Animal; D005434:Flow Cytometry; D006965:Hyperplasia; D007136:Immunoglobulins / Q000378:metabolism*; D051379:Mice; D009000:Monocytes / Q000473:pathology*; D017539:Tunica Intima / Q000378:metabolism / Q000473:pathology*
D015815:Cell Adhesion Molecules; D007136:Immunoglobulins; C486723:Jam3 protein, mouse