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Published on: September 11, 2017
MiR-124 Reduced Neuroinflammation after Traumatic Brain Injury by Inhibiting TRAF6
Yongxiang Yang1,2, Yuqin Ye2,3, Kexia Fan1
1Department of Neurosurgery, The General Hospital of Western Theater Command, Chengdu, China.
Introduction:
Neuroinflammation contributes to secondary injury after traumatic brain injury (TBI), which has been mainly mediated by the microglia. MiR-124 was reported to play an important role in the polarization of microglia by targeting TLR4 signaling pathway. However, the role and mechanism of miR-124 in neuroinflammation mediated by microglia after TBI is unclear. To clarify this, we performed this research.
Methods:
The expression of miR-124 was first measured by RT-PCR in the injured brain at 1/3/7 days post-TBI. Then, miR-124 mimics or inhibitors administration was used to interfere the expression of miR-124 at 24 h post-TBI. Subsequently, the microglia polarization markers were detected by RT-PCR, the expression of inflammatory cytokines was detected by ELISA, the expression of TLR4/MyD88/IRAK1/TRAF6/NF-κB was measured by WB, and the neurological deficit was evaluated by NSS and MWM test. At last, in vitro experiments were performed to explore the exact target molecule of miR-124 on TLR4 signaling pathway.
Results:
Animal research indicated that the expression of miR-124 was downregulated after TBI. Upregulation of miR-124 promoted the M2 polarization of microglia and inhibited the activity of TLR4 pathway, as well as reduced neuroinflammation and neurological deficit after TBI. In vitro experiments indicated that miR-124 promoted the M2 polarization of microglia and reduced neuroinflammation by inhibiting TRAF6.
Conclusion:
This study demonstrated that upregulation of miR-124 promoted the M2 polarization of microglia and reduced neuroinflammation after TBI by inhibiting TRAF6.
Insights
Upregulating miR-124 in traumatic brain injury (TBI) promotes beneficial M2 microglia polarization and reduces neuroinflammation by inhibiting TRAF6, improving neurological deficits.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Neuroinflammation, primarily mediated by microglia, exacerbates secondary injury following traumatic brain injury (TBI).
- MicroRNA-124 (miR-124) is implicated in microglial polarization via the Toll-like receptor 4 (TLR4) signaling pathway, but its precise role in TBI-induced neuroinflammation remains unclear.
Purpose of the Study:
- To elucidate the role and underlying mechanism of miR-124 in TBI-induced neuroinflammation mediated by microglia.
- To investigate the therapeutic potential of modulating miR-124 expression in TBI.
Main Methods:
- Quantitative real-time PCR (RT-PCR) to measure miR-124 expression post-TBI.
- Administration of miR-124 mimics or inhibitors to modulate miR-124 levels in vivo.
- Assessment of microglial polarization markers, inflammatory cytokines (ELISA), and TLR4 signaling pathway components (Western blot).
- Evaluation of neurological deficits using the neurological severity score (NSS) and Morris water maze (MWM) tests.
- In vitro experiments to identify miR-124's direct target in the TLR4 pathway.
Main Results:
- miR-124 expression was significantly downregulated in the injured brain after TBI.
- Upregulation of miR-124 promoted M2 microglial polarization and suppressed the TLR4 signaling pathway.
- miR-124 inhibition of TRAF6 was identified as a key mechanism for reducing neuroinflammation.
- Enhanced miR-124 levels led to reduced neuroinflammation and improved neurological function in TBI models.
Conclusions:
- Upregulation of miR-124 mitigates TBI-induced neuroinflammation and neurological deficits.
- The mechanism involves promoting M2 microglial polarization and inhibiting the TRAF6 protein within the TLR4 signaling pathway.
