دورية أكاديمية

MiR-199-3p Suppressed Inflammatory Response by Targeting MECP2 to Alleviate RTX-Induced PHN in Mice

التفاصيل البيبلوغرافية
العنوان: MiR-199-3p Suppressed Inflammatory Response by Targeting MECP2 to Alleviate RTX-Induced PHN in Mice
المؤلفون: Zhijian Wang, Wei Shen, Mengye Zhu, Mu Xu, Mizhen Qiu, Daying Zhang, Shibiao Chen
المصدر: Cell Transplantation, Vol 31 (2022)
بيانات النشر: SAGE Publishing, 2022.
سنة النشر: 2022
المجموعة: LCC:Medicine
مصطلحات موضوعية: Medicine
الوصف: 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 RTX 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. Increased thermal withdrawal latency (TWL) and decreased mechanical withdrawal threshold (MWT) were observed 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 RTX-induced PHN in mice.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1555-3892
09636897
Relation: https://doaj.org/toc/1555-3892
DOI: 10.1177/09636897221108192
URL الوصول: https://doaj.org/article/cf38d7b73d614570b95bb2fd11a4459d
رقم الأكسشن: edsdoj.f38d7b73d614570b95bb2fd11a4459d
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:15553892
09636897
DOI:10.1177/09636897221108192