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Excessive autophagy contributes to neuron death in cerebral ischemia.

Authors: Shi, R  Weng, J  Zhao, L  Li, XM  Gao, TM  Kong, J 
Citation: Shi R, etal., CNS Neurosci Ther. 2012 Mar;18(3):250-60. doi: 10.1111/j.1755-5949.2012.00295.x.
Pubmed: (View Article at PubMed) PMID:22449108
DOI: Full-text: DOI:10.1111/j.1755-5949.2012.00295.x

AIMS: To determine the extent to which autophagy contributes to neuronal death in cerebral hypoxia and ischemia. METHODS: We performed immunocytochemistry, western blot, cell viability assay, and electron microscopy to analyze autophagy activities in vitro and in vivo. RESULTS: In both primary cortical neurons and SH-SY5Y cells exposed to oxygen and glucose deprivation (OGD)for 6 h and reperfusion (RP) for 24, 48, and 72 h, respectively, an increase of autophagy was observed as determined by the increased ratio of LC3-II to LC3-I and Beclin-1 (BECN1) expression. Using Fluoro-Jade C and monodansylcadaverine double-staining, and electron microscopy we found the increment in autophagy after OGD/RP was accompanied by increased autophagic cell death, and this increased cell death was inhibited by the specific autophagy inhibitor, 3-methyladenine. The presence of large autolysosomes and numerous autophagosomes in cortical neurons were confirmed by electron microscopy. Autophagy activities were increased dramatically in the ischemic brains 3-7 days postinjury from a rat model of neonatal cerebral hypoxia/ischemia as shown by increased punctate LC3 staining and BECN1 expression. CONCLUSION: Excessive activation of autophagy contributes to neuronal death in cerebral ischemia.

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RGD Object Information
RGD ID: 6483050
Created: 2012-05-11
Species: All species
Last Modified: 2012-05-11
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.