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Alzheimer's Disease, Other Dementia, Aging

開催日 2014/9/13
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Wnt1 inducible signaling pathway protein1(WISP1) による抗アポトーシスシグナル経路を介した神経保護作用の可能性について
Wnt1 inducible signaling pathway protein1(WISP1) may prevent neuronal injury through anti-apoptosis signaling

  • P3-277
  • 上田 かりん / Karin Ueda:1 渡邊 究 / Kiwamu Watanabe:2 前迫 真人 / Masato Maesako:1 植村 健吾 / Kengo Uemura:2 上村 麻衣子 / Maiko Uemura:2 秋山  治彦 / Haruhiko Akiyama:3 浅田 めぐみ / Megumi Asada:1 高橋 良輔 / Ryosuke Takahashi:2 下濱 俊 / Shun Shimohama:4 木下 彩栄 / Ayae Kinoshita:1 
  • 1:京都大学大学院医学研究科人間健康科学系専攻 / Department of Human Health Science, Kyoto University Graduate School of Medicine, Kyoto, Japan 2:京都大学医学研究科臨床神経学 / Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan 3:東京都医学総合研 / Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan 4:札幌医大医神経内科 / Department of Neurology, Sapporo Medical University, Hokkaido, Japan 

Wnt1 inducible signaling pathway protein1(WISP1), a member of the CCN family, is widely known as a key factor which regulates cell proliferation, cytoprotection, and ECM production. It is expressed in both epithelial and mesenchymal cells, known to be involved in cardiomyocyte death, osteoarthritis, and carcinomas such as breast cancer and colon tumor. Its mRNA level or protein expression is reported to be increased in above diseases, suggesting that WISP1 is deeply associated with various pathological conditions. Although the expression of WISP1 is reported to be low in the adult brain, several reports have recently suggested that its expression level is increased in microglia under stress conditions including oxidant stress. Further, Aβ42, which is a pathological peptide in Alzheimer's disease(AD), is reported to induce WISP1 expression in microglia. Thus, in order to make clear the role of WISP1 on the pathogenesis of AD, we first examined the expression level of WISP1 in the AD brains or in the amyloid precursor protein(APP)-transgenic mouse brains by ELISA. Interestingly, the WISP1 expression level tended to be increased in the AD brains or in the APP mouse brains compared to the controls. Moreover, in the wild type(control) mouse brains, the WISP1 expression was decreased in an age-dependent manner, though the age-dependent reduction was attenuated in the APP mouse brains. Next, using the stable expressing cell line of WISP1, we explored whether WISP1 up-regulates PI3-K/Akt1 pathway, because it has been suggested WISP1 prevents cell death through PI3-K/Akt1 pathway which further regulates GSK-3β, β-catenin, caspase-3, or mTOR. Dynamics of this stream when WISP1 is overexpressed stably is still under research. Our results indicate that WISP1 is involved in physiological response against Aβ42 toxicity and reduction of its expression may accelerate AD progression.

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