Regulation of integrin α6 recycling by calcium-independent phospholipase A2 (iPLA2) to promote microglia chemotaxis on laminin = iPLA2에 의한 인테그린 Alpha-6의 리사이클링 조절은 소교세포의 이동성을 촉진

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Title
Regulation of integrin α6 recycling by calcium-independent phospholipase A2 (iPLA2) to promote microglia chemotaxis on laminin = iPLA2에 의한 인테그린 Alpha-6의 리사이클링 조절은 소교세포의 이동성을 촉진
Author(s)
Sang Hyun Lee; N Sud; N Lee; S Subramaniyam; C Y Chung
Bibliographic Citation
Journal of Biological Chemistry, vol. 291, no. 45, pp. 23645-23653
Publication Year
2016
Abstract
Microglia are the immune effector cells that are activated in response to pathological changes in the central nervous system. Microglial activation is accompanied by the alteration of integrin expression on the microglia surface. However, changes of integrin expression upon chemoattractant (ADP) stimulation still remain unknown. In this study, we investigated whether ADP induces the alteration of integrin species on the cell surface, leading to changes in chemotactic ability on different extracellular matrix proteins. Flow cytometry scans and on-cell Western assays showed that ADP stimulation induced a significant increase of α6 integrin-GFP, but not α5, on the surface of microglia cells. Microglia also showed a greater motility increase on laminin than fibronectin after ADP stimulation. Time lapse microscopy and integrin endocytosis assay revealed the essential role of calcium-independent phospholipase A2 activity for the recycling of α6 integrin-GFP from the endo-somal recycling complex to the plasma membrane. Lack of calcium-independent phospholipase A2 activity caused a reduced rate of focal adhesion formation on laminin at the leading edge. Our results suggest that the alteration of integrin-mediated adhesion may regulate the extent of microglial infiltration into the site of damage by controlling their chemotactic ability.
ISSN
0021-9258
Publisher
Amer Soc Biochemistry Molecular Biology Inc
DOI
http://dx.doi.org/10.1074/jbc.M116.732610
Type
Article
Appears in Collections:
Division of Biomedical Research > Biotherapeutics Translational Research Center > 1. Journal Articles
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