Authors

H. Yao; R. Ma; L. Yang; G. Hu; X. F. Chen; M. Duan; Y. Kook; F. Niu; K. Liao; M. G. Fu; G. Hu; P. Kolattukudy;S. Buch

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Abbreviated Journal Title

Nat. Commun.

Keywords

TRANSCRIPTION FACTOR; MULTIPLE-SCLEROSIS; BRAIN-INJURY; AGED MICE; IN-VIVO; MICRORNA-9; EXPRESSION; MACROPHAGES; DIFFERENTIATION; PROLIFERATION; Multidisciplinary Sciences

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-kappa B pathway, but not the beta-catenin pathway.

Journal Title

Nature Communications

Volume

5

Publication Date

1-1-2015

Document Type

Article

Language

English

First Page

12

WOS Identifier

WOS:000340618700001

ISSN

2041-1723

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