Abstract:
:Macrophage polarization is a dynamic and integral process of tissue inflammation and remodeling. Here we demonstrate an important role of Aurora kinase A in the regulation of inflammatory M1 macrophage polarization. We found that there was an elevated expression of Aurora-A in M1 macrophages and inhibition of Aurora-A by small molecules or specific siRNA selectively led to the suppression of M1 polarization, sparing over the M2 macrophage differentiation. At the molecular level, we found that the effects of Aurora-A in M1 macrophages were mediated through the down-regulation of NF-κB pathway and subsequent IRF5 expression. In an autoimmune disease model, experimental autoimmune encephalitis (EAE), treatment with Aurora kinase inhibitor blocked the disease development and shifted the macrophage phenotype from inflammatory M1 to anti-inflammatory M2. Thus, this study reveals a novel function of Aurora-A in controlling the polarization of macrophages, and modification of Aurora-A activity may lead to a new therapeutic approach for chronic inflammatory diseases.
journal_name
Inflammationjournal_title
Inflammationauthors
Ding L,Gu H,Gao X,Xiong S,Zheng Bdoi
10.1007/s10753-014-9990-2subject
Has Abstractpub_date
2015-04-01 00:00:00pages
800-11issue
2eissn
0360-3997issn
1573-2576journal_volume
38pub_type
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