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Published on: May 22, 2019
MiR-199-3p Suppressed Inflammatory Response by Targeting MECP2 to Alleviate TRX-Induced PHN in Mice
Zhijian Wang1, Wei Shen1, Mengye Zhu1
1Department of Pain, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Abstract:
Varicella zoster virus-induced postherpetic neuralgia (PHN) can be alleviated by limited medications with serious side effects. This study aims to investigate the underlying molecular mechanism of miR-199-3p in mediating PHN in mice. 293T cells were transfected with miR-199-3p vectors (mimic/inhibitor). The target relationship between miR-199-3p and MECP2 was confirmed using luciferase reporter assay. PHN mouse model was established by TRX injection. Animal behaviors were evaluated using Hargreaves test and Von Frey test. Western blot was used for protein analysis, and quantitative reverse transcription polymerase chain reaction was performed for messenger RNA quantification. Serum levels of inflammatory mediators were determined using ELISA. Paw withdrawal latency (PWL) and mechanical withdrawal threshold (MWT) were decreased in resiniferatoxin-induced PHN mice. Downregulated miR-199-3p and upregulated MECP2 were found in PHN mice. Upregulated miR-199-3p increased PWL and MWT, but inhibited MECP2 in PHN mice. Besides, increased miR-199-3p suppressed proinflammatory indicators and activated anti-inflammatory mediators. It also found that MECP2 was the target of miR-199-3p. Further study showed miR-199-3p enhanced PWL and MWT, and supported inflammatory response via targeting MECP2. miR-199-3p regulated inflammation by targeting MECP2 to alleviate TRX-induced PHN in mice.
Insights
MicroRNA-199-3p alleviates postherpetic neuralgia (PHN) in mice by targeting MECP2. This finding offers a potential therapeutic strategy for PHN, a condition with limited treatment options.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Postherpetic neuralgia (PHN), a complication of Varicella zoster virus infection, presents significant challenges due to limited effective treatments and severe side effects.
- Current therapeutic options for PHN are insufficient, necessitating research into novel molecular mechanisms for pain management.
Purpose of the Study:
- To elucidate the role of microRNA-199-3p (miR-199-3p) in the pathogenesis of PHN in a mouse model.
- To investigate the molecular targets and signaling pathways regulated by miR-199-3p in the context of PHN.
Main Methods:
- Establishment of a resiniferatoxin (TRX)-induced PHN mouse model.
- Assessment of nociceptive behavior using Hargreaves and Von Frey tests.
- Molecular analyses including Western blot, quantitative reverse transcription polymerase chain reaction (qRT-PCR), and luciferase reporter assay.
- Quantification of serum inflammatory mediators via ELISA.
Main Results:
- PHN mice exhibited decreased paw withdrawal latency (PWL) and mechanical withdrawal threshold (MWT), alongside downregulated miR-199-3p and upregulated MECP2.
- Overexpression of miR-199-3p in PHN mice significantly improved PWL and MWT, indicating pain alleviation.
- miR-199-3p was confirmed as a direct target of MECP2, and its upregulation suppressed pro-inflammatory mediators while enhancing anti-inflammatory responses.
Conclusions:
- miR-199-3p plays a crucial role in alleviating TRX-induced PHN in mice by targeting and inhibiting MECP2.
- The miR-199-3p/MECP2 axis modulates neuroinflammation, presenting a potential therapeutic target for managing PHN.
