A novel human foamy virus mediated gene transfer of GAD67 reduces neuropathic pain following spinal cord injury

Liu, Wanhong; Liu, Zhongchun; Liu, Li; Xiao, Zheman; Cao, Xiaofeng; Cao, Zhijian; Lü, Xue; Miao, Lei; He, Xiaohua; Li, Wenxin

doi:10.1016/j.neulet.2007.11.054

Cited by 44 publications

(45 citation statements)

References 17 publications

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“…Total RNA was extracted from spinal dorsal horn tissue using TRIzol reagent (Invitrogen). RNA labeling and hybridization on miRNA microarray chips were conducted as described previously (Liu et al, 2004a). Briefly, the purified RNA using the mirVANA miRNA Isolation Kit (Applied Biosystems) was labeled with fluorescein and hybridization was performed on miRNA microarray chips (miRNA microarray V4.0; CapitalBio) containing 1965 probes in triplicate.…”

Section: Methodsmentioning

confidence: 99%

mir-500-Mediated GAD67 Downregulation Contributes to Neuropathic Pain

et al. 2016

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Neuropathic pain is a common neurobiological disease involving multifaceted maladaptations ranging from gene modulation to synaptic dysfunction, but the interactions between synaptic dysfunction and the genes that are involved in persistent pain remain elusive. In the present study, we found that neuropathic pain induced by the chemotherapeutic drug paclitaxel or L5 ventral root transection significantly impaired the function of GABAergic synapses of spinal dorsal horn neurons via the reduction of the GAD67 expression. We also found that mir-500 expression was significantly increased and involved in the modulation of GAD67 expression via targeting the specific site of Gad1 gene in the dorsal horn. In addition, knock-out of mir-500 or using mir-500 antagomir rescued the GABAergic synapses in the spinal dorsal horn neurons and attenuated the sensitized pain behavior in the rats with neuropathic pain. To our knowledge, this is the first study to investigate the function significance and the underlying molecular mechanisms of mir-500 in the process of neuropathic pain, which sheds light on the development of novel therapeutic options for neuropathic pain.

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Section: Methodsmentioning

confidence: 99%

mir-500-Mediated GAD67 Downregulation Contributes to Neuropathic Pain

et al. 2016

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“…By comparison, 31.6% of the volume transduced with the lentiviral vector maintained long-term expression. Liu et al 33 were of a similar opinion after injecting PFV vector expressing glutamic acid decarboxylase into dorsal root ganglion neuronal cells to attenuate below-injury level central neuropathic pain, after spinal cord injury. Symptoms were reversed after 7 days, reversal lasted for 6 weeks, but re-inoculation with vector was necessary to maintain the restored phenotype for another 6-7 weeks, possibly due to genetic silencing.…”

Section: Genes Delivered By Foamy Virus Vectors In Vivomentioning

confidence: 98%

Progress and prospects: Foamy virus vectors enter a new age

Erlwein

McClure

2010

Gene Ther

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“…To achieve the release of GABA, the GAD67 gene was transferred into dorsal root ganglion (DRG) cells for 7 days after T13 spinal cord hemisection. The result suggests that HFV-mediated gene transfer to DRG could be applied to treat below-injury level central neuropathic pain after incomplete SCI (Liu et al, 2008). The inhibitory effect of GABA, which is the major inhibitory neurotransmitter in the mammalian central nervous system, is mediated by GABA A , GABA B and GABA C /GABA A-ρ receptors (Rissman et al, 2011).…”

Section: Neuropathic Painmentioning

confidence: 99%

“…Neural cells, cultured astrocytes, cultured rat hippocampal and dorsal root ganglia neurons are also transducible by FV vectors (Liu et al, 2005;Liu et al, 2007;Liu et al, 2008). Brain tissues can be transduced by FV vectors in a rat model (Caprariello et al, 2009).…”

Section: Transduction Of Neural Cells and Brain Tissuesmentioning

confidence: 99%