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作 者:Yan-Hu Liang Guo-Wu Chen Xue-Song Li Shu Jia Chun-Yang Meng
机构地区:[1]Department of Clinical Medical College,Jining Medical University,Jining,Shandong Province,China [2]Neuropathic Pain Institute for Spinal Nerve of Jining Medical University,Jining,Shandong Province,China [3]Department of Spine Surgery,Affiliated Hospital of Jining Medical University,Jining,Shandong Province,China [4]Department of Joint Surgery,Yanzhou Campus,Affiliated Hospital of Jining Medical University,Jining,Shandong Province,China
出 处:《Neural Regeneration Research》2021年第3期596-600,共5页中国神经再生研究(英文版)
基 金:supported by the National Natural Science Foundation of China,Nos.81572205 and 81974345(both to CYM)。
摘 要: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 downregulated molecular function.Co-expression network analysis of Mapk14 mRNA and five long noncoding RNAs(lnc RNAs)revealed their correlation.Quantitative reverse transcription-polymerase chain reaction revealed that among five lnc RNAs,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 lnc RNAs 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.
关 键 词:cells factors INFLAMMATION MICROGLIA PAIN pathway protein RNA
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