Journal
REDOX BIOLOGY
Volume 13, Issue -, Pages 665-673Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.redox.2017.08.006
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Funding
- Major National Scientific Research Projects [2015CB943100]
- National Natural Science Foundation of China [31330074, 31572378, 31272404]
- National High Technology Research and Development Program of China [2012AA020603]
- Agricultural Science and Technology Innovation Program [ASTIP-IAS05]
- National Institutes of Health [R01AR070752]
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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 Racl-GTPase and PI3IC/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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