Gene therapy for neuropathic pain by silencing of TNF-α expression with lentiviral vectors targeting the dorsal root ganglion in mice.

• Material Type: 博士論文
• ISSN: 1932-6203
• Title: Gene therapy for neuropathic pain by silencing of TNF-α expression with lentiviral vectors targeting the dorsal root ganglion in mice.
• Volume: 9 3
• Author/Editor: OGAWA, Nobuhiro
• Author Heading: OGAWA, Nobuhiro
• Publication, Distribution, etc.: PLoS One
• Publication Date: 2014-03-18
• Publication Date (W3CDTF): 2014-03-18
• Periodical title: PLoS One
• Degree grantor/type: 滋賀医科大学
• Date Granted: 2014-09-10
• Date Granted (W3CDTF): 2014-09-10
• Dissertation Number: 甲第717号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第717号
• Text Language Code: eng
• Target Audience: 一般
• Note (General): Neuropathic pain can be a debilitating condition. Many types of drugs that have been used to treat neuropathic pain have only limited efficacy. Recent studies indicate that pro-inflammatory mediators including tumor necrosis factor α (TNF-α) are involved in the pathogenesis of neuropathic pain. In the present study, we engineered a gene therapy strategy to relieve neuropathic pain by silencing TNF-α expression in the dorsal root ganglion (DRG) using lentiviral vectors expressing TNF short hairpin RNA1-4 (LV-TNF-shRNA1-4) in mice. First, based on its efficacy in silencing TNF-α in vitro, we selected shRNA3 to construct LV-TNF-shRNA3 for in vivo study. We used L5 spinal nerve transection (SNT) mice as a neuropathic pain model. These animals were found to display up-regulated mRNA expression of activating transcription factor 3 (ATF3) and neuropeptide Y (NPY), injury markers, and interleukin (IL)-6, an inflammatory cytokine in the ipsilateral L5 DRG. Injection of LV-TNF-shRNA3 onto the proximal transected site suppressed significantly the mRNA levels of ATF3, NPY and IL-6, reduced mechanical allodynia and neuronal cell death of DRG neurons. These results suggest that lentiviral-mediated silencing of TNF-α in DRG relieves neuropathic pain and reduces neuronal cell death, and may constitute a novel therapeutic option for neuropathic pain.; Thesis or Dissertation; 平成26年度; 10.1371/journal.pone.0092073
• DOI: info:doi/10.1371/journal.pone.0092073; https://doi.org/info:doi/10.1371/journal.pone.0092073
• Persistent ID (NDL): info:ndljp/pid/8952614; https://dl.ndl.go.jp/pid/8952614
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Available (W3CDTF): 2015-03-03
• Date Accepted (W3CDTF): 2015-02-03T05:25:05+09:00
• Date Created (W3CDTF): 2017-02-17
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://hdl.handle.net/10422/7701; https://shiga-med.repo.nii.ac.jp/records/2866
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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