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2020 Fiscal Year Final Research Report

A novel mechanism of astrocyte STAT3 activation and its pathophysiological role

Research Project

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Project/Area Number 19K16260
Research Category

Grant-in-Aid for Early-Career Scientists

Allocation TypeMulti-year Fund
Review Section Basic Section 46010:Neuroscience-general-related
Research InstitutionKyushu University

Principal Investigator

Shiratori-Hayashi Miho (林)  九州大学, 薬学研究院, 助教 (20735641)

Project Period (FY) 2019-04-01 – 2021-03-31
Keywords痒み / 慢性的な痒み / アストロサイト / 脊髄 / STAT3 / カルシウム
Outline of Final Research Achievements

Spinal astrocyte selective IP3R1 knockdown suppressed persistent STAT3 activation, chronic itch and expression of lipocalin-2 (LCN2), an astrocytic STAT3-dependent factor that is required for chronic itch. IL-6-induced IP3R1-dependent astrocytic Ca2+ responses were long-lasting and involved Ca2+ influx through the TRPC channel. Pharmacologic spinal TRPC inhibition attenuated LCN2 expression and chronic itch. IL-6 expression was upregulated in DRG neurons in a mouse model of chronic itch. DRG neuron-selective IL-6 knockdown also attenuated LCN2 expression and chronic itch.

Free Research Field

疼痛学

Academic Significance and Societal Importance of the Research Achievements

本研究によって従来のSTAT3活性化に寄与するシグナルとは異なるカルシウムシグナルとの関連が初めて明らかになったことで,慢性掻痒だけでなく,STAT3の長期的活性化が認められる様々な中枢神経疾患の病態メカニズムのさらなる理解に繋がった。さらに,アストロサイトのSTAT3の長期的活性化には,従来アストロサイトのカルシウムシグナルにおいて重要であると示唆されてきたIP3R2ではなく,IP3R1が選択的に寄与することがわかり,アストロサイトのカルシウムシグナルの新たな一面が明らかになった。

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Published: 2022-01-27  

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