Wip1-dependent modulation of macrophage migration and phagocytosis

Research output: Contribution to journalJournal articleResearchpeer-review


  • Yiting Tang
  • Bing Pan
  • Xin Zhou
  • Kai Xiong
  • Qian Gao
  • Lei Huang
  • Ying Xia
  • Ming Shen
  • Shulin Yang
  • Honglin Liu
  • Tao Tan
  • Jianjie Ma
  • Xuehong Xu
  • Yulian Mu
  • Kui Li

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.

Original languageEnglish
JournalRedox Biology
Pages (from-to)665-673
Number of pages9
Publication statusPublished - 2017

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