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Protective effects of vacuolar H+ -ATPase c on hydrogen peroxide-induced cell death in C6 glioma cells.

Authors: Byun, Yu Jeong  Lee, Seong-Beom  Kim, Dong Jin  Lee, Hwa Ok  Son, Min Jeong  Yang, Chul Woo  Sung, Ki-Wug  Kim, Ho-Shik  Kwon, Oh-Joo  Kim, In-Kyung  Jeong, Seong-Whan 
Citation: Byun YJ, etal., Neurosci Lett. 2007 Oct 2;425(3):183-7. doi: 10.1016/j.neulet.2007.08.027. Epub 2007 Aug 19.
Pubmed: (View Article at PubMed) PMID:17845832
DOI: Full-text: DOI:10.1016/j.neulet.2007.08.027

We have isolated a gene, the c subunit (ATP6L) of vacuolar H(+)-ATPase, involved in oxidative stress response. In this study, we examined the role of ATP6L and its molecular mechanisms in glial cell death induced by H(2)O(2). Expression of the ATP6L gene was increased by H(2)O(2) treatment in C6 glial cells. ATP6L siRNA-transfected C6 cells treated with H(2)O(2) showed a significant decrease in viability. ATP6L siRNA-transfected cells that were pretreated with MEK1/2 inhibitor completely recovered cell viability. Pretreatment of the transfected cells with zVAD-fmk, a pan-specific caspase inhibitor, did not result in the recovery of cell viability, as determined by a H(2)O(2)-induced cytotoxicity assay. The ultrastructural morphology of the transfected cells as seen by the use of transmission electron microscopy showed numerous cytoplasmic autophagic vacuoles with double membrane. These results suggest that ATP6L has a protective role against H(2)O(2)-induced cytotoxicity via an inhibition of the Erk1/2 signaling pathway, leading to inhibition of autophagic cell death.

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CRRD Object Information
CRRD ID: 14700553
Created: 2019-08-06
Species: All species
Last Modified: 2019-08-06
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.