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MiR-124 contributes to M2 polarization of microglia and confers brain inflammatory protection via the C/EBP-α pathway in intracerebral hemorrhage

Yu, Anyong, Zhang, Tianxi, Duan, Haizhen, Pan, Yong, Zhang, Xiaojun, Yang, Guang, Wang, Juan, Deng, Yi, Yang, Zhao·2017·Immunology Letters

Abstract

Microglia mediated inflammation contributes to intracerebral hemorrhage (ICH) induced secondary injury. Activated microglia has dual functions as pro-inflammatory (M1) and anti-inflammatory (M2) factors in brain injury and repair. MiR-124 is a potent anti-inflammatory agent which affects microglia after brain injury. However, the potential of modulating the M1/M2 polarization of microglia after ICH has not been reported. In this experiment, we detected the effect of miR-124 on the M1/M2 polarization state. In addition, the ability miR-124 to subsequently impacted neurological deficit and cerebral water content of ICH mice were studied. Furthermore, the relationship between miR-124 and C/EBP-α target was detected. We found that miR-124 significantly increased in M2-polarized microglia. Transduction of miR-124 mimics decreased proinflammatory cytokine levels. A coculture model of microglia and neuron indicated that M2-polarized microglia protected neuron damage. Furthermore, miR-124 banded to the 3-untranslated region of C/EBP-α and downregulated its protein levels. In vivo, infusion of miR-124 decreased brain levels of C/EBP-α and significantly reduced brain injury in ICH mice. Thus, miR-124 ameliorated ICH-induced inflammatory injury by modulating microglia polarization toward the M2 phenotype via C/EBP-α. MiR-124 regulatory mechanisms also might represent new therapeutic strategy in ICH.

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Metadata

Authors
Yu, A., Zhang, T., Duan, H., Pan, Y., Zhang, X., Yang, G., Wang, J., Deng, Y., & Yang, Z.
Venue
Immunology Letters
Publisher
Elsevier BV
Published
2017-02
Volume
182
Pages
1-11
ISSN
0165-2478
Cited by
107
References
5
Language
en
Funders
NSFC (81560217)

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