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KAKEN_17K18093seika.pdf
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:Mar 5, 2021 |
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慢性疼痛における神経成長因子シグナリングの解明と新規治療薬の開発
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マンセイ トウツウ ニ オケル シンケイ セイチョウ インシ シグナリング ノ カイメイ ト シンキ チリョウヤク ノ カイハツ
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Mansei tōtsū ni okeru shinkei seichō inshi shigunaringu no kaimei to shinki chiryōyaku no kaihatsu
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Identification of pain-specific nerve growth factor signaling and development of mechanism-based novel therapeutics for chronic pain
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加藤, 純悟
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カトウ, ジュンゴ
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Katō, Jungo
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慶應義塾大学・医学部 (信濃町) ・助教
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Research team head
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科研費研究者番号 : 40465018
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2020
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科学研究費補助金研究成果報告書
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2019
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本研究では、重大な社会問題である慢性疼痛に対し、神経成長因子 (NGF) に着目して新規鎮痛標的の同定を試みた。このNGF変異によって起こる、骨関節の痛覚が特異的に欠如する先天性無痛無汗症V型という疾患に着目し、この疾患のモデルマウスを確立し解析を進めたところ、骨関節の炎症時際に特異的な痛みの欠如が見られた。一方、このNGF変異マウスの唾液腺を調べたところ、NGFは正常に分泌され、組織解析でも神経系の発達も正常であった。さらにこのNGF変異マウスでは炎症時の骨破壊が著しく軽減されることから、このNGF変異が引き起こすシグナリングの変化は骨保護作用のある有力な新規鎮痛標的になりうることが示された。
Chronic pain remains a huge socio-economical problem affecting millions of citizens. We have focused on nerve growth factor (NGF) signaling to identify novel therapeutic targets against chronic pain. In this project, we established a transgenic mouse line that modeled hereditary sensory and autonomic neuropathy type V (HSAN V), in which the NGF mutation results in bone/joint-specific painless phenotype. We observed painless phenotype in the NGF-mutated mice specifically when inflammation takes place in their joints. On the other hand, we found that the maturation and secretion of NGF in salivary gland were normal. The immunohistochemical analysis revealed that the development of pain-related nerve system remained normal in the NGF-mutated mice. Moreover, the bone erosion caused by joint inflammation was significantly attenuated in the NGF-mutated mice. Taken together, the altered NGF signaling taking place in the NGF-mutated mice can be a novel analgesic target for chronic pain.
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研究種目 : 若手研究 (B)
研究期間 : 2017～2019
課題番号 : 17K18093
研究分野 : 麻酔学
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