Wip1-dependent modulation of macrophage migration and phagocytosis

Macrophage accumulation within the vascular wall is a hallmark of atherosclerosis. Controlling macrophage conversion into foam cells remains a major challenge for treatment of atherosclerotic diseases. Here, we show that Wip1, a member of the PP2C family of Ser/Thr protein phosphatases, modulates ma...

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Detalles Bibliográficos
Autores principales: Tang, Yiting, Pan, Bing, Zhou, Xin, Xiong, Kai, Gao, Qian, Huang, Lei, Xia, Ying, Shen, Ming, Yang, Shulin, Liu, Honglin, Tan, Tao, Ma, Jianjie, Xu, Xuehong, Mu, Yulian, Li, Kui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
Research Paper
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562178/
https://www.ncbi.nlm.nih.gov/pubmed/28822916
http://dx.doi.org/10.1016/j.redox.2017.08.006
Descripción
Sumario:Macrophage accumulation within the vascular wall is a hallmark of atherosclerosis. Controlling macrophage conversion into foam cells remains a major challenge for treatment of atherosclerotic diseases. Here, we show that Wip1, a member of the PP2C family of Ser/Thr protein phosphatases, modulates macrophage migration and phagocytosis associated with atherosclerotic plaque formation. Wip1 deficiency increases migratory and phagocytic activities of the macrophage under stress conditions. Enhanced migration of Wip1(-/-) macrophages is mediated by Rac1-GTPase and PI3K/AKT signalling pathways. Elevated phagocytic ability of Wip1(-/-) macrophages is linked to CD36 plasma membrane recruitment that is regulated by AMPK activity. Our study identifies Wip1 as an intrinsic negative regulator of macrophage chemotaxis. We propose that Wip1-dependent control of macrophage function may provide avenues for preventing or eliminating plaque formation in atherosclerosis.

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