Author
Listed:
- 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)
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.
Suggested Citation
Honghong Yao & Rong Ma & Lu Yang & Guoku Hu & Xufeng Chen & Ming Duan & Yeonhee Kook & Fang Niu & Ke Liao & Minggui Fu & Gang Hu & Pappachan Kolattukudy & Shilpa Buch, 2014.
"MiR-9 promotes microglial activation by targeting MCPIP1,"
Nature Communications, Nature, vol. 5(1), pages 1-12, September.
Handle:
RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5386
DOI: 10.1038/ncomms5386
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