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

Yu Jeong Byun; Seong Beom Lee; Dong Jin Kim; Hwa Ok Lee; Min Jeong Son; Chul Woo Yang; Ki Wug Sung; Ho Shik Kim; Oh Joo Kwon; In Kyung Kim; Seong Whan Jeong

doi:10.1016/j.neulet.2007.08.027

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

Yu Jeong Byun
, Seong Beom Lee
, Dong Jin Kim
, Hwa Ok Lee
, Min Jeong Son
, Chul Woo Yang
, Ki Wug Sung
, Ho Shik Kim
, Oh Joo Kwon
, In Kyung Kim
, Seong Whan Jeong

The Catholic University of Korea

Research output: Contribution to journal › Article › peer-review

9 Scopus citations

Abstract

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 H₂O₂. Expression of the ATP6L gene was increased by H₂O₂ treatment in C6 glial cells. ATP6L siRNA-transfected C6 cells treated with H₂O₂ 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 H₂O₂-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 H₂O₂-induced cytotoxicity via an inhibition of the Erk1/2 signaling pathway, leading to inhibition of autophagic cell death.

Original language	English
Pages (from-to)	183-187
Number of pages	5
Journal	Neuroscience Letters
Volume	425
Issue number	3
DOIs	https://doi.org/10.1016/j.neulet.2007.08.027
State	Published - 2 Oct 2007

Bibliographical note

Funding Information:
This work was supported by the Korea Science and Engineering Foundation (KOSEF) through the MRC for Cell Death Disease Research Center at The Catholic University of Korea (R13–2002-005–01003-0). We thank Professor Shin Hee Yoon for technical assistance.

Keywords

Autophagy
Erk
Glia
Hydrogen peroxide
Vacuolar ATPase c

Access to Document

10.1016/j.neulet.2007.08.027

Cite this

@article{50922fc80e304f98b04b2bc6c570e3ee,

title = "Protective effects of vacuolar H+-ATPase c on hydrogen peroxide-induced cell death in C6 glioma cells",

abstract = "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 H2O2. Expression of the ATP6L gene was increased by H2O2 treatment in C6 glial cells. ATP6L siRNA-transfected C6 cells treated with H2O2 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 H2O2-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 H2O2-induced cytotoxicity via an inhibition of the Erk1/2 signaling pathway, leading to inhibition of autophagic cell death.",

keywords = "Autophagy, Erk, Glia, Hydrogen peroxide, Vacuolar ATPase c",

author = "Byun, \{Yu Jeong\} and Lee, \{Seong Beom\} and Kim, \{Dong Jin\} and Lee, \{Hwa Ok\} and Son, \{Min Jeong\} and Yang, \{Chul Woo\} and Sung, \{Ki Wug\} and Kim, \{Ho Shik\} and Kwon, \{Oh Joo\} and Kim, \{In Kyung\} and Jeong, \{Seong Whan\}",

note = "Funding Information: This work was supported by the Korea Science and Engineering Foundation (KOSEF) through the MRC for Cell Death Disease Research Center at The Catholic University of Korea (R13–2002-005–01003-0). We thank Professor Shin Hee Yoon for technical assistance.",

year = "2007",

month = oct,

day = "2",

doi = "10.1016/j.neulet.2007.08.027",

language = "English",

volume = "425",

pages = "183--187",

journal = "Neuroscience Letters",

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TY - JOUR

T1 - Protective effects of vacuolar H+-ATPase c on hydrogen peroxide-induced cell death in C6 glioma cells

AU - Byun, Yu Jeong

AU - Lee, Seong Beom

AU - Kim, Dong Jin

AU - Lee, Hwa Ok

AU - Son, Min Jeong

AU - Yang, Chul Woo

AU - Sung, Ki Wug

AU - Kim, Ho Shik

AU - Kwon, Oh Joo

AU - Kim, In Kyung

AU - Jeong, Seong Whan

N1 - Funding Information: This work was supported by the Korea Science and Engineering Foundation (KOSEF) through the MRC for Cell Death Disease Research Center at The Catholic University of Korea (R13–2002-005–01003-0). We thank Professor Shin Hee Yoon for technical assistance.

PY - 2007/10/2

Y1 - 2007/10/2

N2 - 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 H2O2. Expression of the ATP6L gene was increased by H2O2 treatment in C6 glial cells. ATP6L siRNA-transfected C6 cells treated with H2O2 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 H2O2-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 H2O2-induced cytotoxicity via an inhibition of the Erk1/2 signaling pathway, leading to inhibition of autophagic cell death.

AB - 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 H2O2. Expression of the ATP6L gene was increased by H2O2 treatment in C6 glial cells. ATP6L siRNA-transfected C6 cells treated with H2O2 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 H2O2-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 H2O2-induced cytotoxicity via an inhibition of the Erk1/2 signaling pathway, leading to inhibition of autophagic cell death.

KW - Autophagy

KW - Erk

KW - Glia

KW - Hydrogen peroxide

KW - Vacuolar ATPase c

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U2 - 10.1016/j.neulet.2007.08.027

DO - 10.1016/j.neulet.2007.08.027

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