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Neuronal Death and Neurodegeneration

開催日 2014/9/11
時間 18:00 - 19:00
会場 Room I(311+312)
Chairperson(s) 岡澤 均 / Hitoshi Okazawa (東京医科歯科大学 / Tokyo Medical and Dental University, Japan)
渡部 和彦 / Kazuhiko Watabe (東京都医学総合研究所 神経変性病理 / ALS/Neuropathy Project, Tokyo Metropolitan Institute of Medical Science, Japan)

Mitochondrial fusion and fission proteins expression dynamically change in a murine model of transient ischemic mouse

  • O1-I-6-3
  • 松薗 構佑 / Kosuke Matsuzono:1 劉 文涛 / Wentao Liu:1 菱川 望 / Nozomi Hishikawa:1 山下 徹 / Toru Yamashita:1 出口 健太郎 / Kentaro Deguchi:1 阿部 康二 / Koji Abe:1 
  • 1:岡山大学 / Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical science, Japan 

BACKGROUND: With fusion or fission, mitochondria alter their morphology in response to various physiological and pathological stimuli resulting in either elongated, tubular, interconnected or fragmented form, respectively. In this study, we investigated changes of mitochondrial fission and fusion proteins after transient cerebral ischemia in mice.
METHODS: Immunohistochemistry and Western blot analysis were performed at 2 d, 7 d, 14 d and 28 d after 90 min of transient middle cerebral artery occlusion (tMCAO) in mice.
RESULS: This study first showed that mitochondrial fission protein Dynamin-related protein 1 (Drp1) and fusion protein optic atrophy 1 (Opa1) were both upregulated in the ischemic penumbra with the peak at 2 d after tMCAO, while phosphorylated-Drp1 (P-Drp1) progressively increased with a peak at 14 d after tMCAO. Double immunofluorescent analysis showed many Drp1/cytochrome c oxidase subunit l (COX1) double positive cells and Opa1/COX1 double positive cells in the ischemic penumbra, and also showed some double positive cells with Drp1/terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) and Opa1/TUNEL in the ischemic penumbra. In contrast, both Drp1 and Opa1 showed progressive decreases until 2 d after tMCAO in the ischemic core due to necrotic brain damage.
CONCLUSION: The present study suggests that there happened a continuous mitochondrial fission and fusion during these periods in the ischemic penumbra after tMCAO probably in an effort for mitophagy and cellular survival.

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