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.
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.
Authors: Sakine Simsekyilmaz; Hector A Cabrera-Fuentes; Svenja Meiler; Sawa Kostin; Yvonne Baumer; Elisa A Liehn; Christian Weber; William A Boisvert; Klaus T Preissner; Alma Zernecke Journal: Circulation Date: 2013-11-07 Impact factor: 29.690
Authors: Allison Ostriker; Henrick N Horita; Joanna Poczobutt; Mary C M Weiser-Evans; Raphael A Nemenoff Journal: Arterioscler Thromb Vasc Biol Date: 2014-02-13 Impact factor: 8.311
Authors: Gopala K Yakala; Hector A Cabrera-Fuentes; Gustavo E Crespo-Avilan; Chutima Rattanasopa; Alexandrina Burlacu; Benjamin L George; Kaviya Anand; David Castaño Mayan; Maria Corlianò; Sauri Hernández-Reséndiz; Zihao Wu; Anne M K Schwerk; Amberlyn L J Tan; Laia Trigueros-Motos; Raphael Chèvre; Tricia Chua; Robert Kleemann; Elisa A Liehn; Derek J Hausenloy; Sujoy Ghosh; Roshni R Singaraja Journal: Arterioscler Thromb Vasc Biol Date: 2019-03 Impact factor: 8.311