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Int. J. Mol. Sci. 2016, 17(10), 1770; doi:10.3390/ijms17101770

Annexin-1 Mediates Microglial Activation and Migration via the CK2 Pathway during Oxygen–Glucose Deprivation/Reperfusion

1,2,3,†
,
1,4,†
,
1,2
,
1,2,4
,
1,2
,
1
,
1
and
1,2,*
1
Department of Neurobiology and Key Laboratory of Neurological Diseases of Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, China
2
Institute for Brain Research, Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, China
3
Medical College, Yichun Uiversity, 576 Xuefu Road, Yichun 336000, China
4
Department of Center for Molecular Medicine, Medical College, Hubei University of Arts and Science, Xiangyang 441053, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Academic Editor: Styliani-Anna E. Tsirka
Received: 2 September 2016 / Revised: 11 October 2016 / Accepted: 18 October 2016 / Published: 22 October 2016
(This article belongs to the Special Issue Microglia in Aging and Neurodegenerative Disease)
View Full-Text   |   Download PDF [8841 KB, uploaded 22 October 2016]   |  

Abstract

Annexin-1 (ANXA1) has shown neuroprotective effects and microglia play significant roles during central nervous system injury, yet the underlying mechanisms remain unclear. This study sought to determine whether ANXA1 regulates microglial response to oxygen–glucose deprivation/reperfusion (OGD/R) treatment and to clarify the downstream molecular mechanism. In rat hippocampal slices, OGD/R treatment enhanced the ANXA1 expression in neuron, the formyl peptide receptor (FPRs) expression in microglia, and the microglial activation in the CA1 region (cornu ammonis 1). These effects were reversed by the FPRs antagonist Boc1. The cell membrane currents amplitude of BV-2 microglia (the microglial like cell-line) was increased when treated with Ac2-26, the N-terminal peptide of ANXA1. Ac2-26 treatment enhanced BV-2 microglial migration whereas Boc1 treatment inhibited the migration. In BV-2 microglia, both the expression of the CK2 target phosphorylated α-E-catenin and the binding of casein kinase II (CK2) with α-E-catenin were elevated by Ac2-26, these effects were counteracted by the CK2 inhibitor TBB and small interfering (si) RNA directed against transcripts of CK2 and FPRs. Moreover, both TBB and siRNA-mediated inhibition of CK2 blocked Ac2-26-mediated BV-2 microglia migration. Our findings indicate that ANXA1 promotes microglial activation and migration during OGD/R via FPRs, and CK2 target α-E-catenin phosphorylation is involved in this process. View Full-Text
Keywords: ANXA1; microglia; activation; migration; OGD/R; CK2 ANXA1; microglia; activation; migration; OGD/R; CK2
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Liu, S.; Gao, Y.; Yu, X.; Zhao, B.; Liu, L.; Zhao, Y.; Luo, Z.; Shi, J. Annexin-1 Mediates Microglial Activation and Migration via the CK2 Pathway during Oxygen–Glucose Deprivation/Reperfusion. Int. J. Mol. Sci. 2016, 17, 1770.

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