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MiR-124 Enriched Exosomes Promoted the M2 Polarization of Microglia and Enhanced Hippocampus Neurogenesis After Traumatic Brain Injury by Inhibiting TLR4 Pathway

Yang, Yongxiang, Ye, Yuqin, Kong, Chuiguang, Su, Xinhong, Zhang, Xin, Bai, Wei, He, Xiaosheng·2019·Neurochemical Research
DOI 10.1007/s11064-018-02714-z
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Abstract

MicroRNA-124 (miR-124) is a brain specific miRNA that is highly expressed in microglia. The upregulation of miR-124 contributes to M2 polarization of microglia, which is beneficial to neurogenesis. Exosomes are lipid membrane vesicles that can deliver miR-124 into the brain. However, whether miR-124 enriched exosomes (Exo-miR-124) can regulate the polarization of microglia and affect hippocampus neurogenesis after traumatic brain injury (TBI) is unknown. To clarify this, the Exo-miR-124 was first constructed, and then was intravenously administrated into rats via tail vein with the dose of 3 × 10 9 particles/each rat at 24 h post TBI. The polarization of microglia in hippocampus was evaluated through measuring the signature genes and cytokines of M1/M2 phenotype by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immune sorbent assay (ELISA) at 7/14/21/28 days after TBI. Hippocampus neurogenesis was evaluated through detecting the proliferation marker BrdU/SOX2 and differentiation marker BrdU/NeuN by immunofluorescence (IF) at 7 and 28 days after TBI respectively. Neurological function was evaluated by neurological severity score (NSS) and morris water maze (MWM) at 7/14/21/28 and 24-28 days after TBI respectively. To explore the underlying mechanisms, the mRNA expression of TLR4 pathway molecules in hippocampus were measured by RT-PCR, and the polarization of microglia and the activation of TLR4 pathway in BV2 cells were measured after exosome treat…

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Metadata

Authors
Yang, Y., Ye, Y., Kong, C., Su, X., Zhang, X., Bai, W., & He, X.
Venue
Neurochemical Research
Publisher
Springer Science and Business Media LLC
Published
2019-01-09
Volume
44
Issue
4
Pages
811-828
ISSN
  • 0364-3190
  • 1573-6903
DOI
10.1007/s11064-018-02714-z
Cited by
194
References
6
Language
en
Licence
www.springer.com/tdm (tdm)

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