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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Suppression of miR-155 attenuates neuropathic pain by inducing an M1 to M2 switch in microglia
Yanxiang Zhang1, Qi Chen1, Yu Nai1
1Department of Neurology, Yantai Yuhuangding Hospital, China.
Introduction:
The polarization state of microglia affects the progress of neuropathic pain. MiR-155 modulates polarization of microglia, while its role in neuropathic pain has not been well studied.
Material And Methods:
We separately used lipopolysaccharide (LPS) and interleukin 4 (IL-4) for constructing an M1/M2 polarization model in BV-2 cells. The levels of CD86, iNOS, CD206, Arg and miR-155 were measured by western blot or qRT-PCR, as needed. Subsequently, BV-2 cells were transfected with miR-155 mimics or inhibitor to explore the effects of miR-155 on polarization states. We also constructed a neuropathic pain model by applying spinal nerve ligation (SNL) in Wistar rats with miR-155 agomir or antagomir injection. The withdrawal threshold was measured by Von Frey fibre needle. The levels of interleukin 1b (IL-1b), tumour necrosis factor a (TNF-a) and the proportion of M1-polarized microglia in primary microglia from rats were measured by ELISA and flow cytometry.
Results:
LPS induced M1 polarization in BV-2 cells with increasing of CD86, iNOS and miR-155, while IL-4 induced M2 polarization in BV-2 cells with increasing of CD206, Arg and decreasing of miR-155. MiR-155 mimics upregulated CD86 and downregulated CD206, whereas miR-155 inhibitor downregulated CD86 and upregulated CD206. MiR-155 antagomir increased the withdrawal threshold, decreased the production of IL-1b, TNF-a and the proportion of M1-polarized microglia in primary microglia.
Conclusions:
Results demonstrate that suppression of miR-155 attenuates neuropathic pain by inducing an M1 to M2 switch in microglia. Our findings provide a new perspective to understand the function of miR-155 in microglia.
Insights
Suppression of miR-155 alleviates neuropathic pain by shifting microglia from M1 to M2 polarization. This study reveals miR-155
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Microglial polarization significantly influences neuropathic pain progression.
- MicroRNA-155 (miR-155) is implicated in microglial polarization, but its specific role in neuropathic pain remains understudied.
Purpose of the Study:
- To investigate the role of miR-155 in modulating microglial polarization and its impact on neuropathic pain.
Main Methods:
- Established M1/M2 microglial polarization models in BV-2 cells using lipopolysaccharide (LPS) and interleukin-4 (IL-4).
- Assessed microglial polarization markers (CD86, iNOS, CD206, Arg) and miR-155 levels.
- Utilized miR-155 mimics/inhibitors in cell cultures and miR-155 agomir/antagomir in a rat spinal nerve ligation (SNL) model of neuropathic pain.
- Measured pain withdrawal thresholds, pro-inflammatory cytokines (IL-1β, TNF-α), and M1 microglia proportion.
Main Results:
- LPS induced M1 polarization (increased CD86, iNOS, miR-155), while IL-4 induced M2 polarization (increased CD206, Arg, decreased miR-155).
- miR-155 mimics promoted M1 markers, and inhibitors promoted M2 markers.
- In vivo, miR-155 antagomir treatment reduced pain sensitivity, decreased IL-1β and TNF-α levels, and lowered the M1 microglia proportion.
Conclusions:
- Suppression of miR-155 effectively attenuates neuropathic pain.
- This attenuation is achieved by promoting a switch from M1 to M2 microglial polarization.
- These findings offer novel insights into miR-155's function in microglial regulation and neuropathic pain.
