Abstract
Microglia activation has been implicated in the pathogenesis of many neurological diseases. These reactive microglia are capable of producing a variety of proinflammatory mediators and potentially neurotoxic compounds. The increase of cell number and expression of CD11b are the main features of activated microglia. In this study, we examined the suppressive effects of CDK11p58 on microglia activation induced by lipopolysaccharide (LPS) in vitro. We found that in the activated microglia, the expression of CDK11p58 increased and the overexpression of CDK11p58 could reduce the increased proliferation and CD11b expression in LPS-activated microglia. Such suppressive effects might be resulted from the interaction with cyclin D3 which promoted CDK11p58 nuclear localization. Our results suggested that CDK11p58 acted to regulate microglia activation through CDK11p58 and cyclin D3 interaction.
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Acknowledgments
This work was supported by grants from Chinese National Natural Science Foundation (Nos 81401124), Social Science and Technology Innovation and Demonstration Foundation of Nantong City (MS22015003); Preventive Medicine Projects from Bureau of Jiangsu Province (Y2012083);“Top Six Types of Talents” Financial Assistance of Jiangsu Province (Grant no. 10.WSN016).
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Biyu Shen and Tianyu Gu contributed equally to this work
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Shen, B., Gu, T., Chen, H. et al. CDK11p58 Promotes Microglia Activation via Inducing Cyclin D3 Nuclear Localization. Inflammation 40, 636–644 (2017). https://doi.org/10.1007/s10753-017-0510-z
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DOI: https://doi.org/10.1007/s10753-017-0510-z