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The neuroimmune guidance cue netrin-1 promotes atherosclerosis by inhibiting the emigration of macrophages from plaques
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The neuroimmune guidance cue netrin-1 promotes atherosclerosis by inhibiting the emigration of macrophages from plaques
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Journal Article
The neuroimmune guidance cue netrin-1 promotes atherosclerosis by inhibiting the emigration of macrophages from plaques
2012
Overview
Lipid-engorged macrophages accumulate in atherosclerotic plaques where chronic inflammation ensues. Moore and colleagues show that macrophage migration to chemokines and egress is arrested by netrin-1, which is secreted in the plaque lesions.
Atherosclerotic plaque formation is fueled by the persistence of lipid-laden macrophages in the artery wall. The mechanisms by which these cells become trapped, thereby establishing chronic inflammation, remain unknown. Here we found that netrin-1, a neuroimmune guidance cue, was secreted by macrophages in human and mouse atheroma, where it inactivated the migration of macrophages toward chemokines linked to their egress from plaques. Acting via its receptor, UNC5b, netrin-1 inhibited the migration of macrophages directed by the chemokines CCL2 and CCL19, activation of the actin-remodeling GTPase Rac1 and actin polymerization. Targeted deletion of netrin-1 in macrophages resulted in much less atherosclerosis in mice deficient in the receptor for low-density lipoprotein and promoted the emigration of macrophages from plaques. Thus, netrin-1 promoted atherosclerosis by retaining macrophages in the artery wall. Our results establish a causative role for negative regulators of leukocyte migration in chronic inflammation.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animals
/ Atherosclerosis - immunology
/ Biomedical and Life Sciences
/ Chemokine CCL19 - metabolism
/ Humans
/ Mice
/ Nerve Growth Factors - genetics
/ Nerve Growth Factors - metabolism
/ Netrin-1
/ Plaque, Atherosclerotic - immunology
/ rac GTP-Binding Proteins - metabolism
/ rac1 GTP-Binding Protein - metabolism
/ Receptors, Cell Surface - metabolism
