Induction of Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) Expression in Rat Brain after Focal Ischemia/Reperfusion

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  • Ryota Tanaka
    Department of Neurology, Juntendo University School of Medicine, Tokyo
  • Hideki Mochizuki
    Department of Neurology, Juntendo University School of Medicine, Tokyo
  • Asuka Suzuki
    Department of Neurology, Juntendo University School of Medicine, Tokyo
  • Nobuo Katsube
    Minase Research Institute, Ono Pharmaceutical Co., Ltd., Mishima, Osaka
  • Ryoichi Ishitani
    Group on Cellular Neurobiology, Josai University, Sakado, Saitama, Japan
  • Yoshikuni Mizuno
    Department of Neurology, Juntendo University School of Medicine, Tokyo
  • Takao Urabe
    Department of Neurology, Juntendo University School of Medicine, Tokyo

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<jats:p> Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a glycolytic enzyme, has been recently identified to be involved in the initiation of neuronal apoptosis. To investigate the serial changes and cellular localization of GAPDH expression, and its role in ischemia/reperfusion-induced neuronal apoptosis, the authors analyzed immunohistochemically brain areas of rats subjected to middle cerebral artery occlusion (MCAO) and reperfusion. Nuclear overexpression of GAPDH was noted in the ischemic core area after 2 hours of MCAO without reperfusion. During the subsequent reperfusion, nuclear accumulation of GAPDH in this area decreased in a time-dependent manner. However, cytoplasmic and nuclear GAPDH immunoreactivity was detected in neurons of the penumbra area of the parietal cortex, in rats subjected to 2-hour MCAO followed by 3-hour reperfusion. The increase of nuclear GAPDH immunoreactivity was persistently noted up to 48 hours of reperfusion, whereas cytoplasmic immunoreactivity correlated inversely with the duration of reperfusion. Moreover, double staining revealed colocalization of nuclear GAPDH and TUNEL in the penumbra area. The authors' study demonstrated that overexpression of GAPDH and nuclear translocation occurred in both the ischemic core and penumbra area soon after focal ischemia. These processes could be viewed as an early marker of ischemia/reperfusion-induced apoptotic neuronal death. The results suggest that GAPDH may play a critical role in the progression and spread of ischemic neuronal damage. </jats:p>

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