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Bcl-x L blocks mitochondrial multiple conductance channel activation and inhibits 6-OHDA-induced death in SH-SY5Y cells

Jordán, Joaquín; Galindo, María F; Tornero, Daniel LU ; González-García, Carmen and Ceña, Valentín (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
publishing date
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
  • 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
2017-01-01 08:22:31
@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},
  keyword      = {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},
  volume       = {89},
  year         = {2004},
}