在慢性收缩性损伤大鼠模型中,LncRNA PCAT19通过调控miR-182-5p/JMJD1A调控神经性疼痛。

IF 2.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Neuroimmunomodulation Pub Date : 2022-01-01 Epub Date: 2021-09-09 DOI:10.1159/000518847
Miao Huo, Xingxing Zheng, Ning Bai, Ruifen Xu, Guang Yang, Ziyu Zhao
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引用次数: 4

摘要

神经性疼痛(NP)是最严重的慢性疼痛类型之一。近年来,越来越多的研究表明,长链非编码RNA (LncRNA)在包括NP在内的多种人类疾病中发挥着关键作用。然而,LncRNA前列腺癌相关转录本19 (PCAT19)在NP中的作用及其具体机制尚不清楚。方法:建立慢性收缩性损伤(CCI)大鼠模型。采用足爪戒断阈值和足爪戒断潜伏期评价模型大鼠神经元疼痛行为。采用实时荧光定量PCR检测PCAT19、神经炎症因子、microRNA (miR)-182-5p、含巨梦基结构域1A (JMJD1A) mRNA表达。ELISA法检测炎症因子蛋白表达。采用双荧光素酶报告基因法评价基因间的靶向关系。结果:CCI大鼠PCAT19持续上调。miR-182-5p是PCAT19的靶标,PCAT19敲低后miR-182-5p升高。通过敲除PCAT19可减少机械性异位痛、热痛觉过敏等NP行为以及神经炎症。然而,注射miR-182-5p拮抗剂可显著逆转PCAT19敲低引起的NP行为和神经炎症水平。此外,双荧光素酶报告基因实验显示,JMJD1A是miR-182-5p的靶基因。CCI大鼠JMJD1A水平随时间增加而升高。PCAT19敲除后,JMJD1A显著降低,但抑制miR-182-5p可逆转其水平。结论:本研究表明PCAT19通过靶向miR-182-5p/JMJD1A轴在NP中发挥作用,PCAT19可作为NP新的治疗靶点。
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LncRNA PCAT19 Regulates Neuropathic Pain via Regulation of miR-182-5p/JMJD1A in a Rat Model of Chronic Constriction Injury.

Introduction: Neuropathic pain (NP) is one of the most severe chronic pain types. In recent years, more and more studies have shown that long noncoding RNA (LncRNA) plays a key role in a variety of human diseases, including NP. However, the role of LncRNA prostate cancer-associated transcript 19 (PCAT19) in NP and its specific mechanism remain unclear.

Methods: A chronic constrictive injury (CCI) rat model was established. Rat paw withdrawal threshold and paw withdrawal latency were used to evaluate the neuronal pain behavior of rats in this model. mRNA expression of PCAT19, neuroinflammatory factor, microRNA (miR)-182-5p, and Jumonji domain containing 1A (JMJD1A) were detected by quantitative real-time PCR. ELISA analysis was used to detect inflammatory factor protein expression. Dual-luciferase reporter assay was used to evaluate the targeting relationship between genes.

Results: PCAT19 was continuously upregulated in CCI rats. miR-182-5p was the target of PCAT19, and miR-182-5p was increased after PCAT19 knockdown. NP behaviors such as mechanical ectopic pain and thermal hyperalgesia as well as neuroinflammation can be reduced by knocking down PCAT19. However, the injection of miR-182-5p antagomir significantly reversed the level of the NP behaviors and neuroinflammation caused by PCAT19 knockdown. Besides, dual-luciferase reporter assay showed that JMJD1A was the target gene of miR-182-5p. The level of JMJD1A in CCI rats increased with time. After PCAT19 knockdown, JMJD1A was significantly decreased, but inhibition of miR-182-5p can reverse its levels.

Conclusion: This study shows that PCAT19 plays a role in NP by targeting the miR-182-5p/JMJD1A axis, and PCAT19 can be used as a new therapeutic target for NP.

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来源期刊
Neuroimmunomodulation
Neuroimmunomodulation 医学-免疫学
CiteScore
3.60
自引率
4.20%
发文量
35
审稿时长
>12 weeks
期刊介绍: The rapidly expanding area of research known as neuroimmunomodulation explores the way in which the nervous system interacts with the immune system via neural, hormonal, and paracrine actions. Encompassing both basic and clinical research, ''Neuroimmunomodulation'' reports on all aspects of these interactions. Basic investigations consider all neural and humoral networks from molecular genetics through cell regulation to integrative systems of the body. The journal also aims to clarify the basic mechanisms involved in the pathogenesis of the CNS pathology in AIDS patients and in various neurodegenerative diseases. Although primarily devoted to research articles, timely reviews are published on a regular basis.
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