Wip1-dependent modulation of macrophage migration and phagocytosis

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

doi:10.1016/j.redox.2017.08.006

Wip1-dependent modulation of macrophage migration and phagocytosis

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

^*Corresponding author for this work

7 Citations (Scopus)

48 Downloads (Pure)

Abstract

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 language	English
Journal	Redox Biology
Volume	13
Pages (from-to)	665-673
Number of pages	9
ISSN	2213-2317
DOIs	https://doi.org/10.1016/j.redox.2017.08.006
Publication status	Published - 2017

Access to Document

10.1016/j.redox.2017.08.006Licence: CC BY-NC-ND

1-s2.0-S2213231717304159-mainFinal published version, 1.37 MBLicence: CC BY-NC-ND

Cite this

@article{f744b0331d1e41fdb9dee2833fa42b4d,

title = "Wip1-dependent modulation of macrophage migration and phagocytosis",

abstract = "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.",

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

year = "2017",

doi = "10.1016/j.redox.2017.08.006",

language = "English",

volume = "13",

pages = "665--673",

journal = "Redox Biology",

issn = "2213-2317",

publisher = "Elsevier",

}

TY - JOUR

T1 - Wip1-dependent modulation of macrophage migration and phagocytosis

AU - Tang, Yiting

AU - Pan, Bing

AU - Zhou, Xin

AU - Xiong, Kai

AU - Gao, Qian

AU - Huang, Lei

AU - Xia, Ying

AU - Shen, Ming

AU - Yang, Shulin

AU - Liu, Honglin

AU - Tan, Tao

AU - Ma, Jianjie

AU - Xu, Xuehong

AU - Mu, Yulian

AU - Li, Kui

PY - 2017

Y1 - 2017

N2 - 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.

AB - 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.

U2 - 10.1016/j.redox.2017.08.006

DO - 10.1016/j.redox.2017.08.006

M3 - Journal article

C2 - 28822916

AN - SCOPUS:85027512302

SN - 2213-2317

VL - 13

SP - 665

EP - 673

JO - Redox Biology

JF - Redox Biology

ER -

Wip1-dependent modulation of macrophage migration and phagocytosis

Abstract

Access to Document

Fingerprint

Cite this