MiR-9 promotes microglial activation by targeting MCPIP1

Honghong Yao, Rong Ma, Lu Yang, Guoku Hu, Xufeng Chen, Ming Duan, Yeonhee Kook, Fang Niu, Ke Liao, Minggui Fu, Gang Hu, Pappachan Kolattukudy and Shilpa Buch ()
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Honghong Yao: Medical School of Southeast University
Rong Ma: University of Nebraska Medical Center
Lu Yang: University of Nebraska Medical Center
Guoku Hu: University of Nebraska Medical Center
Xufeng Chen: The first Affiliated Hospital of Nanjing Medical University
Ming Duan: Key Laboratory for Zoonosis Research, Ministry of Education, Jilin University
Yeonhee Kook: University of Nebraska Medical Center
Fang Niu: University of Nebraska Medical Center
Ke Liao: University of Nebraska Medical Center
Minggui Fu: School of Medicine, University of Missouri-Kansas City
Gang Hu: Jiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University
Pappachan Kolattukudy: Burnett School of Biomedical Science, College of Medicine, University of Central Florida
Shilpa Buch: University of Nebraska Medical Center

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: Abstract Microglia participate in innate inflammatory responses within the central nervous system. The highly conserved microRNA-9 (miR-9) plays critical roles in neurogenesis as well as axonal extension. Its role in microglial inflammatory responses, however, remains poorly understood. Here we identify a unique role of miR-9 in mediating the microglial inflammatory response via distinct signalling pathways. MiR-9-mediated regulation of cellular activation involved downregulated expression of the target protein, monocyte chemotactic protein-induced protein 1 (MCPIP1) that is crucial for controlling inflammation. Results indicate that miR-9-mediated cellular activation involved signalling via the NF-κB pathway, but not the β-catenin pathway.

Date: 2014
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DOI: 10.1038/ncomms5386

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