Elucidation of the role of calpain on the degeneration of spines caused by diabetes using a low molecular weight compound

使用低分子量化合物阐明钙蛋白酶对糖尿病引起的脊柱变性的作用

• 批准号: 21700414
• 负责人: KOSUGE Yasuhiro
• 金额: $ 2.75万
• 依托单位: Nihon University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21700414/
• 关键词: 糖尿病; 海馬; スパイン; カルパイン; シナプス可塑性

Chronic hyperglycemia, such as diabetes mellitus, has been shown to induce cognitive impairment and defects of long-term potentiation in the hippocampus. In order to assess the mechanism of cognitive impairment by hyperglycemia, the expression of post-synaptic density 95 (PSD-95), a key components of spine, was investigated in a human neruoblastoma cell line, SH-SY5Y, after exposure to high-glucose and in the hippocampus in streptozotocin-induced diabetic mice. These results suggest that decrease in phosphorylated ERK plays a significant role in the adverse effect of chronic hyperglycemia in vivo and in vitro.

慢性高血糖（例如糖尿病）已被证明会诱导海马中长期增强的认知障碍和缺陷。为了评估高血糖的认知障碍的机制，在人的内鲁母细胞瘤细胞系中研究了突触后密度95（PSD-95）的表达（PSD-95）是脊柱的关键成分，SH-SY5Y，暴露于高葡萄糖后，在高葡萄糖和海马疗法蛋白毒素中。这些结果表明，磷酸化的ERK的降低在体内和体外的慢性高血糖的不良影响中起着重要作用。

项目成果

ストレプトゾトシン誘発糖尿病マウス海馬における細胞内シグナル伝達系の変化

链脲佐菌素诱导糖尿病小鼠海马细胞内信号转导系统的变化

• 发表时间: 2010
• 作者: 小菅康弘;川島由樹;山岡由佳;山岸由佳;宮岸寛子;石毛久美子;伊藤芳久
• 通讯作者: 伊藤芳久

Characterization of chronic glutamate-mediated motor neuron toxicity in organotypic spinal cord culture prepared from ALS model mice

• DOI: 10.1016/j.neulet.2009.03.017
• 发表时间: 2009-04-24
• 期刊: NEUROSCIENCE LETTERS
• 影响因子: 2.5
• 作者: Kosuge, Yasuhiro;Sekikawa-Nishida, Kayo;Ito, Yoshihisa
• 通讯作者: Ito, Yoshihisa