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鸟苷-5'-三磷酸环水解酶1调控的长链非编码RNA是神经性疼痛中微胶质细胞激活的潜在靶点。

Guanosine-5'-triphosphate cyclohydrolase 1 regulated long noncoding RNAs are potential targets for microglial activation in neuropathic pain.

作者信息

Liang Yan-Hu, Chen Guo-Wu, Li Xue-Song, Jia Shu, Meng Chun-Yang

机构信息

Department of Clinical Medical College, Jining Medical University; Neuropathic Pain Institute for Spinal Nerve of Jining Medical University, Jining, Shandong Province, China.

Neuropathic Pain Institute for Spinal Nerve of Jining Medical University; Department of Spine Surgery, Affiliated Hospital of Jining Medical University, Jining, Shandong Province, China.

出版信息

Neural Regen Res. 2021 Mar;16(3):596-600. doi: 10.4103/1673-5374.290914.

DOI:10.4103/1673-5374.290914
PMID:32985494
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7996028/
Abstract

Several studies have confirmed that microglia are involved in neuropathic pain. Inhibition of guanosine-5'-triphosphate cyclohydrolase 1 (GTPCH1) can reduce the inflammation of microglia. However, the precise mechanism by which GTPCH1 regulates neuropathic pain remains unclear. In this study, BV2 microglia were transfected with adenovirus to knockdown GTPCH1 expression. High throughput sequencing analysis revealed that the mitogen-activated protein kinase (MAPK) related pathways and proteins were the most significantly down-regulated molecular function. Co-expression network analysis of Mapk14 mRNA and five long noncoding RNAs (lncRNAs) revealed their correlation. Quantitative reverse transcription-polymerase chain reaction revealed that among five lncRNAs, ENSMUST00000205634, ENSMUST00000218450 and ENSMUST00000156079 were related to the downregulation of Mapk14 mRNA expression. These provide some new potential targets for the involvement of GTPCH1 in neuropathic pain. This study is the first to note the differential expression of lncRNAs and mRNA in GTPCH1 knockdown BV2 microglia. Findings from this study reveal the mechanism by which GTPCH1 activates microglia and provide new potential targets for microglial activation in neuropathic pain.

摘要

多项研究证实，小胶质细胞参与神经性疼痛。抑制鸟苷-5'-三磷酸环水解酶1（GTPCH1）可减轻小胶质细胞的炎症反应。然而，GTPCH1调节神经性疼痛的确切机制仍不清楚。在本研究中，用腺病毒转染BV2小胶质细胞以敲低GTPCH1表达。高通量测序分析显示，丝裂原活化蛋白激酶（MAPK）相关途径和蛋白是下调最显著的分子功能。对Mapk14 mRNA和5种长链非编码RNA（lncRNA）进行共表达网络分析，揭示了它们之间的相关性。定量逆转录-聚合酶链反应显示，在5种lncRNA中，ENSMUST00000205634、ENSMUST00000218450和ENSMUST00000156079与Mapk14 mRNA表达下调有关。这些为GTPCH1参与神经性疼痛提供了一些新的潜在靶点。本研究首次指出GTPCH1敲低的BV2小胶质细胞中lncRNA和mRNA的差异表达。本研究结果揭示了GTPCH1激活小胶质细胞的机制，并为神经性疼痛中小胶质细胞激活提供了新的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbb5/7996028/8276a82d2bf9/NRR-16-596-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbb5/7996028/a5a28a610fa6/NRR-16-596-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbb5/7996028/44a91afdd1c8/NRR-16-596-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbb5/7996028/8276a82d2bf9/NRR-16-596-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbb5/7996028/a5a28a610fa6/NRR-16-596-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbb5/7996028/44a91afdd1c8/NRR-16-596-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbb5/7996028/8276a82d2bf9/NRR-16-596-g004.jpg

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