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MafB promotes atherosclerosis by inhibiting foam-cell apoptosis
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Journal Article
MafB promotes atherosclerosis by inhibiting foam-cell apoptosis
2014
Overview
MafB is a transcription factor that induces myelomonocytic differentiation. However, the precise role of MafB in the pathogenic function of macrophages has never been clarified. Here we demonstrate that MafB promotes hyperlipidemic atherosclerosis by suppressing foam-cell apoptosis. Our data show that MafB is predominantly expressed in foam cells found within atherosclerotic lesions, where MafB mediates the oxidized LDL-activated LXR/RXR-induced expression of apoptosis inhibitor of macrophages (AIM). In the absence of MafB, activated LXR/RXR fails to induce the expression of AIM, a protein that is normally responsible for protecting macrophages from apoptosis; thus,
Mafb
-deficient macrophages are prone to apoptosis. Haematopoietic reconstitution with
Mafb
-deficient fetal liver cells in recipient LDL receptor-deficient hyperlipidemic mice revealed accelerated foam-cell apoptosis, which subsequently led to the attenuation of the early atherogenic lesion. These findings represent the first evidence that the macrophage-affiliated MafB transcription factor participates in the acceleration of atherogenesis.
In the early stages of atherosclerosis, macrophages in the vessel wall convert into foam cells, which promote the rise of atherosclerotic plaques. Here Hamada
et al
. show that the macrophage transcription factor MafB inhibits foam-cell apoptosis, and that its absence promotes atherosclerosis development in mice.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/51
/ 13/89
/ 14/35
/ 38/61
/ 64/60
/ Animals
/ Apoptosis Regulatory Proteins - genetics
/ Atherosclerosis - physiopathology
/ Humanities and Social Sciences
/ Humans
/ Lesions
/ Low density lipoprotein receptors
/ MafB Transcription Factor - genetics
/ MafB Transcription Factor - physiology
/ Medicine
/ Mice
/ Orphan Nuclear Receptors - metabolism
/ Receptors, Immunologic - genetics
/ Retinoid X Receptors - metabolism
/ Science
