Neuronal cell death mediated by mitochondria

线粒体介导的神经细胞死亡

• 批准号: 21659018
• 负责人: YONEDA Yukio
• 金额: $ 2.1万
• 依托单位: Kanazawa University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Challenging Exploratory Research
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21659018/
• 关键词: ミトコンドリア; 神経細胞死; NMDA; グルタミン酸; 脳虚血; NMDAレセプター; UCP2; 人口チャネル; Ca2+蛍光イメージング; NMDA受容体; ミトコンドリア膜電位; ミトコンドリア内カルシウム濃度; mPTP; 海馬神経細胞; 細胞内遊離カルシウム濃度

Glutamate neurotoxicity was found to at least in part involve mitochondrial membrane potential disruption, mPTP orchestration, mitochondrial free Ca^<2+> levels and UCP2 expression in rat hippocampal and cortical neurons. In HEK293 cells with acquired NMDAR channels and overexpressed UCP2, a more marked increase was seen in mitochondrial free Ca^<2+> levels, in addition to more severe cell death, after the exposure to NMDA than in cells without UCP2 overexpression. Accordingly, UCP2 could play a role as a determinant of the neurotoxicity mediated by NMDAR through a mechanism related to the modulation of mitochondrial free Ca^<2+> levels in neurons.

谷氨酸神经毒性至少部分涉及大鼠海马和皮层神经元线粒体膜电位破坏、mPTP协调、线粒体游离Ca^2+水平和UCP2表达。在具有获得性NMDAR通道和UCP2过表达的HEK293细胞中，与没有UCP2过表达的细胞相比，在暴露于NMDA后，除了更严重的细胞死亡外，还观察到线粒体游离Ca^2+水平更显著的增加。因此，UCP2可能通过调节神经元线粒体游离Ca^2+水平的机制，在NMDAR介导的神经毒性中发挥决定性作用。

项目成果

Natural polyamines spermidine and spermine prevent bone loss through preferential disturbance of osteoclastic activation in ovariectomized mice

天然多胺亚精胺和精胺通过优先干扰卵巢切除小鼠的破骨细胞活化来防止骨质流失

• 发表时间: 2012
• 期刊: Br J Pharmacol
• 作者: Yamamoto T;Hinoi E;Fujita H;Iezaki T;Takahata Y;Takamori M & Yoneda Y
• 通讯作者: Takamori M & Yoneda Y

A pivotal role of mitochondrial free calcium in neurotoxicity mediated by pN-methyl-D-aspartate receptors in cultured rat hippocampal neurons.

线粒体游离钙在培养的大鼠海马神经元中 pN-甲基-D-天冬氨酸受体介导的神经毒性中发挥关键作用。

• 发表时间: 2011
• 期刊: Neurochem Int
• 影响因子: 4.2
• 作者: Yukari Nakamura;Eiichi Hinoi;Takeshi Takarada;Yoshifumi Takahata;Tomomi Yamamoto;Hiroyuki Fujita;Saya Takada;Syota Hashizume;Yukio Yoneda;Kambe Y
• 通讯作者: Kambe Y

Behavioral abnormality and pharmacologic response in social isolation-reared mice

• DOI: 10.1016/j.bbr.2009.03.028
• 发表时间: 2009-08-24
• 期刊: BEHAVIOURAL BRAIN RESEARCH
• 影响因子: 2.7
• 作者: Koike, Hiroyuki;Ibi, Daisuke;Yamada, Kiyofumi
• 通讯作者: Yamada, Kiyofumi

Amelioration by the Natural Polyamine Spermine of Cartilage and Bone Destruction in Rats With Collagen-Induced Arthritis

• DOI: 10.1254/jphs.11241sc
• 发表时间: 2012-05-01
• 期刊: JOURNAL OF PHARMACOLOGICAL SCIENCES
• 影响因子: 3.5
• 作者: Iezaki, Takashi;Hinoi, Eiichi;Yoneda, Yukio
• 通讯作者: Yoneda, Yukio

Functional expression of beta2 adrenergic receptors responsiblefor protection against oxidative stress through promotion of glutathione synthesis after Nrf2 upregulation in undifferentiated mesenchymal C3H10T1/2 stem cells

未分化间充质 C3H10T1/2 干细胞中 Nrf2 上调后，β2 肾上腺素受体的功能表达负责通过促进谷胱甘肽合成来防止氧化应激

• 发表时间: 2008
• 期刊: J Cell Physiol 218
• 作者: Yoshifumi Takahata;Takeshi Takarada;Mika lemata;Tomomi Yamamoto;Yukary Nakamura;Ayumi Kodama and Yukio Yoneda
• 通讯作者: Ayumi Kodama and Yukio Yoneda