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- Title
Nogo-66 inhibits adhesion and migration of microglia via GTPase Rho pathway in vitro.
- Authors
Yan, Jun; Zhou, Xiao; Guo, Jing-Jing; Mao, Lei; Wang, Yi-Jin; Sun, Jing; Sun, Li-Xin; Zhang, Lu-Yong; Zhou, Xin-Fu; Liao, Hong
- Abstract
J. Neurochem. (2012) 120, 721-731. Abstract Nogo-66 is a 66-amino-acid-residue extracellular domain of Nogo-A, which plays a key role in inhibition neurite outgrowth of central nervous system through binding to the Nogo-66 receptor (NgR) expressed on the neuron. Recent studies have confirmed that NgR is also expressed on the surface of macrophages/microglia in multiple sclerosis, but its biological effects remain unknown. In the present study, our results demonstrated that Nogo-66 triggered microglia anti-adhesion and inhibited their migration in vitro, which was mediated by NgR. We also assessed the roles of small GTP (glycosyl phosphatidylinositol)-binding proteins of the Rho family as the downstream signal transducers on the microglia adhesion and mobility induced by Nogo-66. The results showed that Nogo-66 activated RhoA and reduced the activity of Cdc42 in the meanwhile, which further triggered the anti-adhesion and migration inhibition effects to microglia. Nogo-66 inhibited microglia polarization and membrane protrusion formation, thus might eventually contribute to the decreasing capability of cell mobility. Taken together, the Nogo-66/NgR pathway may modulate neuroinflammation via mediating microglia adhesion and migration in addition to its role in neurons. Better understanding the relationship between Nogo-66/NgR and neuroinflammation may help targeting NgR for treating central nervous system diseases related with inflammation.
- Subjects
CENTRAL nervous system; MICROGLIA; ADHESION; VITRONECTIN; EMIGRATION &; immigration
- Publication
Journal of Neurochemistry, 2012, Vol 120, Issue 5, p721
- ISSN
0022-3042
- Publication type
Article
- DOI
10.1111/j.1471-4159.2011.07619.x