体内转染(Entranster)与大鼠神经病理性疼痛研究.docVIP

体内转染(Entranster)与大鼠神经病理性疼痛研究.doc

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Long noncoding RNA MRAK009713is a novel regulator of neuropathic pain in rats Guilin Li a ,Huaide Jiang a ,Chaoran Zheng a ,Gaochun Zhu b ,Yurong Xu a ,Xuan Sheng a ,Bing Wu a ,Jingjing Guo a ,Shuanghua Zhu c ,Yuting Zhan c ,Weijian Lin c ,Rui Ding c ,Chunping Zhang d ,Shuangmei Liu a ,Lifang Zou a ,Zhihua Yi a ,Shangdong Liang a,* 1.Introduction Long noncoding RNAs (lncRNAsare .200nt RNA molecules 4,30that exert distinct functions in a variety of biological processes in a manner independent of protein translation.4,34For instance,lncRNAs participate in posttranscriptional gene regulation by controlling protein synthesis,RNA maturation and transport,and transcriptional gene silencing through the modification of chromatin structure.34,36,39LncRNAs can also act in cis at the site of transcription or in trans to drive region-,locus-or allele-specific transcription.2,21It is important that the expression of lncRNAs is often more tissue-or cell type-specific than that of protein-coding genes.22Studies using genetic knockout animal models have indicated that multiple lncRNAs function in disease pathogenesis.20,22,27,29Furthermore,experimental evidence supports the development of disease therapies targeting lncRNAs.2,15,38However,the pathological roles of lncRNAs in vivo remain unclear. Hyperresponsiveness to external nociceptive stimuli in primary sensory neuron afferents and central synapses results in sensitization,which underlies both neuropathic and inflammatory chronic pain.6,8,11Neuropathic pain is notoriously difficult to treat with currently available analgesics.Molecular and cellular alterations in primary sensory neurons after peripheral nerve injury play important roles in the pathogenesis of neuropathic pain.17,24Although lncRNAs have been implicated in many pathological injury processes in the nervous system,28only a small number of lncRNAs have been functionally identified so far,and their roles in neuropathic pain are not well understood.1 Here,we ident

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