Journal
CELL DEATH & DISEASE
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41419-018-0821-5
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Funding
- National Natural Science Foundation of China [81671240, 81371397, 81560220, 81701711]
- Guangdong Provincial Clinical Medical Centre for Neurosurgery [2013B020400005]
- Youth Science Fund of Jiangxi Province [20151BAB215014]
- Key project of Jiangxi Youth Science Foundation [20171ACB21054]
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The role of microglial-mediated sustained neuroinflammation in the onset and progression of Parkinson's disease (PD) is well established, but the mechanisms contributing to microglial activation remain unclear. LincRNA-p21, a well studied long intergenic noncoding RNA (lincRNA), plays pivotal roles in diverse biological processes and diseases. Its role in microglial activation and inflammation-induced neurotoxicity, however, has not yet been fully elucidated. Here, we report that lincRNA-p21 promotes microglial activation through a p53-dependent transcriptional pathway. We further demonstrate that lincRNA-p21 competitively binds to the miR-181 family and induces microglial activation through the miR-181/PKC-delta pathway. Moreover, PKC-delta induction further increases the expression of p53/lincRNA-p21 and thus forms a circuit. Taken together, our results suggest that p53/lincRNA-p21, together with miR-181/PKC-delta, form a double-negative feedback loop that facilitates sustained microglial activation and the deterioration of neurodegeneration.
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