Role of oxidative stress in the apoptotic cell death of cultured cerebellar granule neurons

2001 ◽  
Vol 64 (3) ◽  
pp. 284-297 ◽  
Author(s):  
Antonio Valencia ◽  
Julio Morán
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cerebellar Granule Neurons ◽  
Granule Neurons ◽  
Cerebellar Granule

Role of Ionic Fluxes in the Apoptotic Cell Death of Cultured Cerebellar Granule Neurons

2004 ◽  
Vol 29 (1) ◽  
pp. 227-238 ◽  
Author(s):  
A. Franco-Cea ◽  
A. Valencia ◽  
S. Sánchez-Armass ◽  
G. Domínguez ◽  
J. Morán
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cerebellar Granule Neurons ◽  
Granule Neurons ◽  
Cerebellar Granule ◽  
Ionic Fluxes

Lysophosphatidylcholine protects cerebellar granule neurons from apoptotic cell death

2009 ◽  
Vol 87 (1) ◽  
pp. 190-199 ◽  
Author(s):  
Yutaka Ikeno ◽  
So-hyun Cheon ◽  
Naoko Konno ◽  
Ayako Nakamura ◽  
Katsuhiko Kitamoto ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cerebellar Granule Neurons ◽  
Granule Neurons ◽  
Cerebellar Granule

Apoptotic cell death of cerebellar granule neurons in genetically ataxia (ax) mice

2000 ◽  
Vol 288 (3) ◽  
pp. 167-170 ◽  
Author(s):  
Makoto Ohgoh ◽  
Kazuto Yamazaki ◽  
Hiroo Ogura ◽  
Yukio Nishizawa ◽  
Isao Tanaka
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cerebellar Granule Neurons ◽  
Granule Neurons ◽  
Cerebellar Granule

Role of sarcolemmal ATP-sensitive potassium channel in oxidative stress-induced apoptosis: mitochondrial connection

2008 ◽  
Vol 294 (3) ◽  
pp. H1317-H1325 ◽  
Author(s):  
Jasna Marinovic ◽  
Marko Ljubkovic ◽  
Anna Stadnicka ◽  
Zeljko J. Bosnjak ◽  
Martin Bienengraeber
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Specific Interaction ◽  
Protective Role ◽  
Apoptotic Cell Death ◽  
Apoptotic Pathway ◽  
Neonatal Cardiomyocytes ◽  
Channel Inhibition

From time of their discovery, sarcolemmal ATP-sensitive K+ (sarcKATP) channels were thought to have an important protective role in the heart during stress whereby channel opening protects the heart from stress-induced Ca2+ overload and resulting damage. In contrast, some recent studies indicate that sarcKATP channel closing can lead to cardiac protection. Also, the role of the sarcKATP channel in apoptotic cell death is unclear. In the present study, the effects of channel inhibition on apoptosis and the specific interaction between the sarcKATP channel and mitochondria were investigated. Apoptotic cell death of cultured HL-1 and neonatal cardiomyocytes following exposure to oxidative stress was significantly increased in the presence of sarcKATP channel inhibitor HMR-1098 as evidenced by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling and caspase-3,7 assays. This was paralleled by an increased release of cytochrome c from mitochondria to cytosol, suggesting activation of the mitochondrial death pathway. sarcKATP channel inhibition during stress had no effect on Bcl-2, Bad, and phospho-Bad, indicating that the increase in apoptosis cannot be attributed to these modulators of the apoptotic pathway. However, monitoring of mitochondrial Ca2+ with rhod-2 fluorescent indicator revealed that mitochondrial Ca2+ accumulation during stress is potentiated in the presence of HMR-1098. In conclusion, this study provides novel evidence that opening of sarcKATP channels, through a specific Ca2+-related interaction with mitochondria, plays an important role in preventing cardiomyocyte apoptosis and mitochondrial damage during stress.

Sign in / Sign up

Export Citation Format

Share Document