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Downregulation of miR-199b promotes the acute spinal cord injury through IKKβ-NF-κB signaling pathway activating microglial cells

Zhou, Heng-Jun, Wang, Li-Qing, Xu, Qing-Sheng, Fan, Zuo-Xu, Zhu, Yu, Jiang, Hao, Zheng, Xiu-Jue, Ma, Yue-Hui, Zhan, Ren-Ya·2016·Experimental Cell Research
DOI 10.1016/j.yexcr.2016.09.020
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Abstract

Inflammatory response played an important role in the progression of spinal cord injury (SCI). Several miRNAs were associated with the pathology of SCI. However, the molecular mechanism of miRNA involving in inflammatory response in acute SCI (ASCI) was poorly understood. Sprague-Dawley (SD) rats were divided into 2 groups: control group (n=6) and acute SCI (ASCI) group (n=6). The expression of miR-199b and IκB kinase β-nuclear factor-kappa B (IKKβ-NF-κB) signaling pathway were evaluated by quantitative reverse transcription-PCR (qRT-PCR) in rats with ASCI and in primary microglia activated by lipopolysaccharide (LPS). We found that downregulation of miR-199b and activation of IKKβ/NF-κB were observed in rats after ASCI and in activated microglia. miR-199b negatively regulated IKKβ by targeting its 3'- untranslated regions (UTR) through using luciferase reporter assay. Overexpression of miR-199b reversed the up-regulation of IKKβ, p-p65, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in LPS-treated BV2 cells assessed by western blotting analysis. In addition, BMS-345541 reversed the up-regulation effects of miR-199b inhibitor on the expression of TNF-α and IL-1β. In the SCI rats, overexpression of miR-199b attenuated ASCI and decreased the expression of IKKβ-NF-κB signaling pathway and TNF-α and IL-1β. These results indicated that miR-199b attenuated ASCI at least partly through IKKβ-NF-κB signaling pathway and affecting the function of microglia. Our findings sug…

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Metadata

Authors
Zhou, H.-J., Wang, L.-Q., Xu, Q.-S., Fan, Z.-X., Zhu, Y., Jiang, H., Zheng, X.-J., Ma, Y.-H., & Zhan, R.-Y.
Venue
Experimental Cell Research
Publisher
Elsevier BV
Published
2016-11
Volume
349
Issue
1
Pages
60-67
ISSN
0014-4827
DOI
10.1016/j.yexcr.2016.09.020
Cited by
64
References
3
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Funders
National Natural Science Foundation of China (81371371)

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