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MafB promotes atherosclerosis by inhibiting foam-cell apoptosis
Michito Hamada1, Megumi Nakamura2, Mai Thi Nhu Tran3
11] Department of Anatomy and Embryology, University of Tsukuba, 1-1-1, Tennodai, Ibaraki 305-8575, Japan [2] International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, 1-1-1, Tennodai, Tsukuba Ibaraki 305-8575, Japan [3] Laboratory Animal Resource Center (LARC), Faculty of Medicine, University of Tsukuba, 1-1-1, Tennodai, Ibaraki 305-8575, Japan [4].
Abstract:
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.
Insights
The transcription factor MafB accelerates atherosclerosis by preventing foam-cell apoptosis in macrophages. MafB deficiency in mice reduces hyperlipidemia and early lesion development, highlighting its role in atherogenesis.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Immunology
Background:
- Macrophages play a critical role in atherosclerosis development.
- Foam cell apoptosis is a key process in regulating atherosclerotic plaque progression.
- The transcription factor MafB's role in macrophage-mediated pathogenesis is not well understood.
Purpose of the Study:
- To elucidate the role of MafB in hyperlipidemic atherosclerosis.
- To investigate MafB's function in foam cell apoptosis and its impact on atherogenesis.
Main Methods:
- Analysis of MafB expression in atherosclerotic lesions.
- Investigating MafB's regulation of apoptosis inhibitor of macrophages (AIM) expression.
- Utilizing hematopoietic reconstitution in LDL receptor-deficient mice to assess MafB's in vivo function.
Main Results:
- MafB is predominantly expressed in foam cells within atherosclerotic lesions.
- MafB mediates the expression of AIM, a crucial apoptosis inhibitor, in response to oxidized LDL.
- Mafb-deficient macrophages exhibit increased apoptosis, leading to attenuated early atherogenesis in hyperlipidemic mice.
Conclusions:
- MafB promotes hyperlipidemic atherosclerosis by suppressing foam cell apoptosis.
- MafB is a key regulator of AIM expression, influencing macrophage survival in atherosclerotic plaques.
- Targeting MafB may offer a novel therapeutic strategy for attenuating atherosclerosis.
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