Novel therapy for neuropathic pain model based on mRNA agerts

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K09455
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 56020:Orthopedics-related
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: Hirai Takashi 東京医科歯科大学, 大学院医歯学総合研究科, 講師 (40510350)
• Co-Investigator(Kenkyū-buntansha): 大川 淳 東京医科歯科大学, 大学院医歯学総合研究科, 教授 (30251507) ; 吉井 俊貴 東京医科歯科大学, 大学院医歯学総合研究科, 准教授 (50583754) ; 位高 啓史 東京医科歯科大学, 生体材料工学研究所, 教授 (60292926)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 神経障害性疼痛 / 脊髄後角 / RNAシーケンス

Outline of Final Research Achievements

We created a mouse neuropathic pain model, excised the dorsal horn of the spinal cord, extracted RNA, and comprehensively investigated gene expression changes using a next-generation sequencer. Approximately 70 types of RNAseq for the dorsal horn of the spinal cord showed changes in expression between the affected side and the Sham model. Of these, 6 genes were upregulated in the SNI model, and these were named genes A to F, respectively. The expression level of gene A was significantly elevated with a difference of about 8000-fold. In addition, the expression level of gene A increased 2.8-fold on the affected side in a comparison of the unaffected side and the affected side in the SNI model. Genes B and F were also significantly elevated in the affected side of the SNI model. On the other hand, it was also found that the expression of about 60 kinds of genes was decreased.

Free Research Field

神経障害性疼痛

Academic Significance and Societal Importance of the Research Achievements

末梢神経障害が生じることで脊髄後角において患側では多くの遺伝子発現が低下することが分かったが、少数の遺伝子では劇的に発現が増加することが分かった。様々な神経障害モデルにおける共通の遺伝子変化を抽出し、メカニズムの原因を突き止めることができれば新たな治療標的として期待できると考えられた。