神经病理性疼痛
竞争性内源性RNA
脊髓
长非编码RNA
实时聚合酶链反应
水通道蛋白4
免疫印迹
免疫组织化学
脊髓损伤
医学
小RNA
分子生物学
化学
核糖核酸
药理学
生物
病理
基因
生物化学
精神科
作者
Shuyue Xian,Ruiwen Ding,Mengyun Li,Feng Chen
标识
DOI:10.1016/j.jneuroim.2020.577457
摘要
Abstract
Background
Neuropathic pain (NP) is the comorbidity in spinal cord injury(SCI), which is the hardest to cure. Non-coding RNA dysregulations are related to the development of NP. NEAT1(nuclear paraspeckle assembly transcript 1) is a new type of lncRNA. This study explores the role and specific mechanism of NEAT1 in SCI-mediated NP. Methods
Firstly, the NEAT1 expression in SCI rats and the control group was detected with RT-PCR to analyze the relationship between NEAT13 and NP symptoms. Then, SCI rats were intrathecally injected with NEAT13 overexpressing and knocking down lentiviruses. Afterward, ELISA was utilized to assess the expression of IL-6, IL-1β and TNFα in rats. Subsequently, immunohistochemistry was adopted to verify the activation of microglial cells. After that, bioinformatics analysis was employed to further predict the downstream target genes of NEAT1, while RT-PCR and Western blot were conducted to determine the relative expression of miR-128-3p and aquaporin-4(AQP4). Meanwhile, a dual-luciferase reporter assay was performed to further study the targeting relationship between NEAT1 and miR-128-3p, and miR-128-3p and AQP4. Results
SCI rats showed distinctly higher NEAT1 expression compared with that of the control group. ELISA experiment confirmed that the over-expression of NEAT1 enhanced the expression of IL-6, IL-1β, and TNFα in SCI rats. Other related mechanism studies revealed that NEAT13 targeted and inhibited miR-128-3p as its competing endogenous RNA (ceRNA), and enhanced AQP4 expression, while miR-128-3p targeted AQP4 to regulate its expression. Summary
NEAT1 affects AQP4 signaling pathway to alleviate the spinal cord injury-induced NP via promoting miR-128-3p expression.
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