Bcl-x L blocks mitochondrial multiple conductance channel activation and inhibits 6-OHDA-induced death in SH-SY5Y cells
(2004) In Journal of Neurochemistry 89(1). p.33-124- Abstract
Apoptosis is an active process that is regulated by different signalling pathways. One of the more important organelles involved in apoptosis regulation is the mitochondrion. Electron chain transport disruption increases free radical production leading to multiple conductance channel opening, release of cytochrome c and caspase activation. This death pathway can be blocked by anti-apoptotic members of the Bcl-2 protein family that might shift redox potential to a more reduced state, preventing free radical-mediated damage. 6-Hydroxydopamine (6-OHDA) has been widely used to generate Parkinson's disease-like models. It is able to generate free radicals and to induce catecholaminergic cell death. In this paper we have used the human... (More)
Apoptosis is an active process that is regulated by different signalling pathways. One of the more important organelles involved in apoptosis regulation is the mitochondrion. Electron chain transport disruption increases free radical production leading to multiple conductance channel opening, release of cytochrome c and caspase activation. This death pathway can be blocked by anti-apoptotic members of the Bcl-2 protein family that might shift redox potential to a more reduced state, preventing free radical-mediated damage. 6-Hydroxydopamine (6-OHDA) has been widely used to generate Parkinson's disease-like models. It is able to generate free radicals and to induce catecholaminergic cell death. In this paper we have used the human neuroblastoma cell line SH-SY5Y overexpressing Bcl-x(L) as a model to gain insights into the mechanisms through which Bcl-x(L) blocks 6-OHDA-induced cell death and to identify the molecular targets for this action. Herein, we present evidence supporting that the Bcl-x(L)-anti-apoptotic signal pathway seems to prevent mitochondrial multiple conductance channel opening, cytochrome c release and caspase-3 like activity following 6-OHDA treatment in the human neuroblastoma cell line SH-SY5Y.
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- author
- Jordán, Joaquín ; Galindo, María F ; Tornero, Daniel LU ; González-García, Carmen and Ceña, Valentín
- publishing date
- 2004-04
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Antioxidants, Apoptosis, Caspase 3, Caspases, Cell Line, Tumor, Cytochromes c, Cytoprotection, Enzyme Activation, Humans, Mitochondria, Neuroblastoma, Oxidopamine, Proto-Oncogene Proteins c-bcl-2, Reactive Oxygen Species, Signal Transduction, bcl-X Protein
- in
- Journal of Neurochemistry
- volume
- 89
- issue
- 1
- pages
- 10 pages
- publisher
- Wiley-Blackwell
- external identifiers
-
- pmid:15030396
- scopus:1842614395
- ISSN
- 0022-3042
- DOI
- 10.1046/j.1471-4159.2003.02299.x
- language
- English
- LU publication?
- no
- id
- 8c2ee4e3-8858-4180-bc29-2deccd02786e
- date added to LUP
- 2016-04-11 15:23:40
- date last changed
- 2024-04-18 21:39:41
@article{8c2ee4e3-8858-4180-bc29-2deccd02786e,
abstract = {{<p>Apoptosis is an active process that is regulated by different signalling pathways. One of the more important organelles involved in apoptosis regulation is the mitochondrion. Electron chain transport disruption increases free radical production leading to multiple conductance channel opening, release of cytochrome c and caspase activation. This death pathway can be blocked by anti-apoptotic members of the Bcl-2 protein family that might shift redox potential to a more reduced state, preventing free radical-mediated damage. 6-Hydroxydopamine (6-OHDA) has been widely used to generate Parkinson's disease-like models. It is able to generate free radicals and to induce catecholaminergic cell death. In this paper we have used the human neuroblastoma cell line SH-SY5Y overexpressing Bcl-x(L) as a model to gain insights into the mechanisms through which Bcl-x(L) blocks 6-OHDA-induced cell death and to identify the molecular targets for this action. Herein, we present evidence supporting that the Bcl-x(L)-anti-apoptotic signal pathway seems to prevent mitochondrial multiple conductance channel opening, cytochrome c release and caspase-3 like activity following 6-OHDA treatment in the human neuroblastoma cell line SH-SY5Y.</p>}},
author = {{Jordán, Joaquín and Galindo, María F and Tornero, Daniel and González-García, Carmen and Ceña, Valentín}},
issn = {{0022-3042}},
keywords = {{Antioxidants; Apoptosis; Caspase 3; Caspases; Cell Line, Tumor; Cytochromes c; Cytoprotection; Enzyme Activation; Humans; Mitochondria; Neuroblastoma; Oxidopamine; Proto-Oncogene Proteins c-bcl-2; Reactive Oxygen Species; Signal Transduction; bcl-X Protein}},
language = {{eng}},
number = {{1}},
pages = {{33--124}},
publisher = {{Wiley-Blackwell}},
series = {{Journal of Neurochemistry}},
title = {{Bcl-x L blocks mitochondrial multiple conductance channel activation and inhibits 6-OHDA-induced death in SH-SY5Y cells}},
url = {{http://dx.doi.org/10.1046/j.1471-4159.2003.02299.x}},
doi = {{10.1046/j.1471-4159.2003.02299.x}},
volume = {{89}},
year = {{2004}},
}