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Cited by 33Cell death mechanisms and regulationRedox biology and oxidative stressProtein Kinase Regulation and GTPase Signaling

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Role of oxidative stress and JNK pathway in apoptotic death induced by potassium deprivation and staurosporine in cerebellar granule neurons

Ramiro-Cortés, Yazmín, Morán, Julio·2009·Neurochemistry International
DOI 10.1016/j.neuint.2009.05.015
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Abstract

Several signaling pathways are differentially activated during apoptotic cell death. We have previously found that during apoptotic death of cerebellar granule neurons (CGN) induced by potassium deprivation (K5) and staurosporine there is an increase in the generation of reactive oxygen species (ROS). The inhibition of ROS generation reduces the extent of cell death. However, remain to be elucidated the mechanisms by which ROS participate in this apoptotic process. On the other hand, it is well known that c-Jun amino-terminal kinase (JNK) pathway plays a pivotal role in cell death of several cell types. In the present study we found that K5 activated the JNK pathway and that its inhibition with SP600125 markedly prevented caspase 3 activation, nuclear condensation and cell death induced by K5. In contrast, JNK pathway was not activated by staurosporine and the JNK inhibitor did not affect cell death induced by this stimulus. We also found that JNK inhibition did not affect ROS levels induced by K5 or staurosporine, suggesting that ROS are upstream of JNK pathway activation. Antioxidants increased ASK1 phosphorylation and decreased JNK1/2 and c-Jun phosphorylation induced by K5. According to these results, we suggest that apoptosis induced by K5 is JNK-dependent and mediated by ROS, but apoptosis induced by staurosporine is not dependent on JNK and that the observed ROS generation by staurosporine seems not to be involved in the activation of this signaling pathway.

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Metadata

Authors
Ramiro-Cortés, Y., & Morán, J.
Affiliations
Universidad Nacional Autónoma de México (MX)
Corresponding author
Morán, Julio
ORCID
Morán, Julio
Venue
Neurochemistry International
Publisher
Elsevier BV
Published
2009-12
Volume
55
Issue
7
Pages
581-592
ISSN
0197-0186 (ISSN-L)
DOI
10.1016/j.neuint.2009.05.015
OpenAlex
W2014294777
Cited by
33
References
2
Citations by year
2024: 2 · 2023: 1 · 2021: 2 · 2020: 2 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 2 · 2014: 4 · 2013: 4 · 2012: 1
FWCI
1.74
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neurochemistry International (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords
oxidative stress, JNK signaling, apoptosis, potassium deprivation, staurosporine, cerebellar granule cells, reactive oxygen species, ASK1, c-Jun phosphorylation, caspase-3, SP600125
MeSH terms
Animals, Antioxidants, Cell Nucleus, Cell Survival, Cerebellum, Enzyme Inhibitors, Glyceraldehyde-3-Phosphate Dehydrogenases, Hypokalemia, Neurons, Blotting, Western, Signal Transduction, Rats, Wistar, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Staurosporine, Kaempferols, JNK Mitogen-Activated Protein Kinases, Rats, Caspase 3

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