| Project/Area Number |
17K14959
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Niigata University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 神経障害性疼痛 / RNA編集 / 脊髄後根神経節 / ADAR / アロディニア / 神経科学 |
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| Outline of Final Research Achievements |
We have previously found that peripheral nerve injury triggers an increase in RNA editing enzyme ADAR2 expression and COPA I/V editing in the dorsal root ganglion, and that ADAR2-deficient mice show a reduction of neuropathic allodynia. The present study was aimed to elucidate the physiological and pathological roles of COPA I/V editing and their regulatory mechanisms. Here we showed that both unedited and edited COPA were primarily located at ER-Golgi intermediate compartment in the transfected HEK293T cells. Also we tried to establish a method to specifically inhibit RNA editing. On the other hand, the present study found that, besides peripheral nerve injury, peripheral inflammation caused an increase in ADAR2 expression and COPA I/V editing in the dorsal root ganglion.
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| Academic Significance and Societal Importance of the Research Achievements |
これまでに本研究代表者は、神経障害性疼痛において、ゲノムの遺伝情報を書き換える「RNA編集」に異常が生じることを見出してきた。本研究課題は、RNA編集異常が痛みの増悪にどのように寄与するかを明らかにするとともに、RNA 編集の人為的操作法の確立を目指す、学術的に意義深いものである。本研究では、炎症による痛みと神経障害性疼痛に共通して、RNA編集異常が生じることも明らかにすることができ、その原因となるメカニズムの理解を進めることができた。
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