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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:1161.)
© 2009 American Heart Association, Inc.

Integrative Physiology/Experimental Medicine

Importance of Junctional Adhesion Molecule-C for Neointimal Hyperplasia and Monocyte Recruitment in Atherosclerosis-Prone Mice–Brief Report

Erdenechimeg Shagdarsuren; Yassin Djalali-Talab; Michel Aurrand-Lions; Kiril Bidzhekov; Elisa A. Liehn; Beat A. Imhof; Christian Weber; Alma Zernecke

From the Institute for Molecular Cardiovascular Research (IMCAR) (E.S., Y.D.-T., K.B., E.A.L., C.W., A.Z.), RWTH Aachen University, Germany; UMR891, Inserm (M.A.-L.), Centre de Recherche en Cancérologie de Marseille, Institut Paoli-Calmettes, France; the Department of Pathology and Immunology (B.A.I.), University Medical Centre, Geneva, Switzerland; and the Rudolf-Virchow-Center (A.Z.), DFG-Research-Center for Experimental Biomedicine, University of Würzburg, Germany.

Correspondence to Dr Alma Zernecke, MD, Institut für Molekulare Herz-Kreislaufforschung, Universitätsklinikum der RWTH Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany. E-mail azernecke{at}ukaachen.de

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.

Methods and 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.

We here show that junctional adhesion molecule (JAM)-C antibody blockade reduced neointimal hyperplasia after arterial injury and leukocyte adhesion to carotid arteries. Our data provide the first evidence for a crucial role of JAM-C in accelerated lesion formation and leukocyte recruitment in atherosclerosis-prone mice.

Key Words: leukocyte recruitment • adhesion molecules • remodeling • inflammation • restonosis • atherosclerosis