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Map3k8 Modulates Monocyte State and Atherogenesis in ApoE-/- Mice
Carlos Sanz-Garcia1, Ángela Sánchez1, Constanza Contreras-Jurado1
1From the Instituto de Investigaciones Biomédicas "Alberto Sols" Madrid, Consejo Superior de Investigaciones Científicas (CSIC-UAM) y Unidad de Biomedicina (UA, CSIC), University of Las Palmas de Gran Canaria, España (C.S.-G., Á.S., C.C.-J., C.C., A.A., S.A.); Departamento de Bioquímica y Biología Molecular y Celular, Facultad de Veterinaria, IISA, University of Zaragoza, España (C.B., J.O.); Instituto de Biomedicina y Biotecnología de Cantabria (CSIC-UC), Santander, España (M.M., R.M.); and Departmento de Farmacologia, Facultad de Medicina, University of Valencia, INCLIVA, España (P.E., M.-J.S.).
Map3k8 deficiency reduces monocyte apoptosis and enhances CCR2 expression, leading to smaller atherosclerotic plaques in mice. This suggests Map3k8 as a potential therapeutic target for atherosclerosis.
Area of Science:
- Immunology
- Molecular Biology
- Cardiovascular Research
Background:
- Map3k8 (Cot/Tpl2) kinase activates MAPK pathways crucial for innate and adaptive immunity.
- Its role in atherogenesis, a complex inflammatory disease, was previously unknown.
Purpose of the Study:
- To investigate the role of Map3k8 in the development of atherosclerosis.
Main Methods:
- Analysis of Map3k8-deficient ApoE-/- mice fed a high-fat diet.
- Assessment of monocyte populations, apoptosis, gene expression, and cellular infiltration in atherosclerotic plaques.
- Bone marrow transplantation experiments.
Main Results:
- Map3k8 deficiency reduced specific monocyte populations and increased their apoptosis.
- Reduced CCR2 expression on circulating monocytes and decreased cellular infiltration in atherosclerotic lesions.
- Map3k8-deficient bone marrow transplantation led to smaller aortic lesions.
Conclusions:
- Map3k8 plays a pro-atherosclerotic role by decreasing monocyte apoptosis and enhancing CCR2 expression.
- Targeting Map3k8 may offer a novel anti-atherosclerotic therapeutic strategy.
