Metabolic activity: A novel indicator of neuronal survival in the murine dopaminergic cell line CAD

Apoptosis is implicated in many neurodegenerative diseases, including Parkinson's disease (PD). Neuroprotective strategies targeting apoptosis need to preserve functional integrity of the saved cells to be effective. The aim of the present study was to evaluate a novel approach for analyzing ne...

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Autores Principales: Arboleda G., Waters C., Gibson R.M.
Formato: Artículo (Article)
Lenguaje:Inglés (English)
Publicado: 2005
Materias:
Cad
Acceso en línea:https://repository.urosario.edu.co/handle/10336/22406
https://doi.org/10.1385/JMN:27:01:65
id ir-10336-22406
recordtype dspace
spelling ir-10336-224062022-05-02T12:37:20Z Metabolic activity: A novel indicator of neuronal survival in the murine dopaminergic cell line CAD Arboleda G. Waters C. Gibson R.M. Biological marker Carbachol Caspase inhibitor Ceramide Muscarinic receptor Neurotrophic factor Neurotrophin 3 Sphingosine derivative Animal cell Apoptosis Article Brain function Catecholamine nerve cell Cell activity Cell death Cell function Cell line Cell metabolism Cell survival Cell viability Central nervous system Dopaminergic nerve cell In vitro study Metabolic activation Molecular model Mouse Nerve cell Nonhuman Parkinson disease Receptor upregulation Amino acid chloromethyl ketones Animals Apoptosis Caspases Cell line Cell survival Cysteine proteinase inhibitors Dopamine Energy metabolism Mice Neurons Neuroprotective agents Neurotrophin 3 Sphingosine Murinae Cad Caspase inhibitor Catecholaminergic cells Ceramide Metabolic activity Microphysiometer Neuronal apoptosis Neurotrophin-3 Apoptosis is implicated in many neurodegenerative diseases, including Parkinson's disease (PD). Neuroprotective strategies targeting apoptosis need to preserve functional integrity of the saved cells to be effective. The aim of the present study was to evaluate a novel approach for analyzing neuronal function that monitors cellular metabolic responses to receptor activation using the microphysiometer. N-Acetyl-sphingosine (C2-ceramide) induced cell death of the neuronal cell line, Cath.a-differentiated (CAD) cells, which resemble catecholaminergic cells of the CNS, and provide a useful in vitro model for the cells affected in PD. C2-ceramide also suppressed the metabolic response of CAD cells to muscarinic receptor activation. Pretreatment with the caspase inhibitor Boc-Asp-(OMe)-fluoromethylketone (BAF) plusneurotrophin-3 (NT-3) reduced C2-ceramide-induced CAD cell death, delaying cell death more effectively than either agent alone; and, most significantly, BAF and NT-3 enabled the cells remaining 24 h after toxin treatment to generate a normal metabolic response to the muscarinic agonist carbachol. On the basis of these results, we suggest that measuring metabolic responses to receptor activation is a useful method for following neuronal viability after toxin treatment and that the combination of caspase inhibitors and neurotrophic factors might be a plausible strategy for improving neuronal survival, with critical preservation of metabolic function. Copyright © 2005 Humana Press Inc. All rights of any nature whatsoever reserved. 2005 2020-05-25T23:56:22Z info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion 8958696 https://repository.urosario.edu.co/handle/10336/22406 https://doi.org/10.1385/JMN:27:01:65 eng info:eu-repo/semantics/openAccess application/pdf instname:Universidad del Rosario
institution EdocUR - Universidad del Rosario
collection DSpace
language Inglés (English)
topic Biological marker
Carbachol
Caspase inhibitor
Ceramide
Muscarinic receptor
Neurotrophic factor
Neurotrophin 3
Sphingosine derivative
Animal cell
Apoptosis
Article
Brain function
Catecholamine nerve cell
Cell activity
Cell death
Cell function
Cell line
Cell metabolism
Cell survival
Cell viability
Central nervous system
Dopaminergic nerve cell
In vitro study
Metabolic activation
Molecular model
Mouse
Nerve cell
Nonhuman
Parkinson disease
Receptor upregulation
Amino acid chloromethyl ketones
Animals
Apoptosis
Caspases
Cell line
Cell survival
Cysteine proteinase inhibitors
Dopamine
Energy metabolism
Mice
Neurons
Neuroprotective agents
Neurotrophin 3
Sphingosine
Murinae
Cad
Caspase inhibitor
Catecholaminergic cells
Ceramide
Metabolic activity
Microphysiometer
Neuronal apoptosis
Neurotrophin-3
spellingShingle Biological marker
Carbachol
Caspase inhibitor
Ceramide
Muscarinic receptor
Neurotrophic factor
Neurotrophin 3
Sphingosine derivative
Animal cell
Apoptosis
Article
Brain function
Catecholamine nerve cell
Cell activity
Cell death
Cell function
Cell line
Cell metabolism
Cell survival
Cell viability
Central nervous system
Dopaminergic nerve cell
In vitro study
Metabolic activation
Molecular model
Mouse
Nerve cell
Nonhuman
Parkinson disease
Receptor upregulation
Amino acid chloromethyl ketones
Animals
Apoptosis
Caspases
Cell line
Cell survival
Cysteine proteinase inhibitors
Dopamine
Energy metabolism
Mice
Neurons
Neuroprotective agents
Neurotrophin 3
Sphingosine
Murinae
Cad
Caspase inhibitor
Catecholaminergic cells
Ceramide
Metabolic activity
Microphysiometer
Neuronal apoptosis
Neurotrophin-3
Arboleda G.
Waters C.
Gibson R.M.
Metabolic activity: A novel indicator of neuronal survival in the murine dopaminergic cell line CAD
description Apoptosis is implicated in many neurodegenerative diseases, including Parkinson's disease (PD). Neuroprotective strategies targeting apoptosis need to preserve functional integrity of the saved cells to be effective. The aim of the present study was to evaluate a novel approach for analyzing neuronal function that monitors cellular metabolic responses to receptor activation using the microphysiometer. N-Acetyl-sphingosine (C2-ceramide) induced cell death of the neuronal cell line, Cath.a-differentiated (CAD) cells, which resemble catecholaminergic cells of the CNS, and provide a useful in vitro model for the cells affected in PD. C2-ceramide also suppressed the metabolic response of CAD cells to muscarinic receptor activation. Pretreatment with the caspase inhibitor Boc-Asp-(OMe)-fluoromethylketone (BAF) plusneurotrophin-3 (NT-3) reduced C2-ceramide-induced CAD cell death, delaying cell death more effectively than either agent alone; and, most significantly, BAF and NT-3 enabled the cells remaining 24 h after toxin treatment to generate a normal metabolic response to the muscarinic agonist carbachol. On the basis of these results, we suggest that measuring metabolic responses to receptor activation is a useful method for following neuronal viability after toxin treatment and that the combination of caspase inhibitors and neurotrophic factors might be a plausible strategy for improving neuronal survival, with critical preservation of metabolic function. Copyright © 2005 Humana Press Inc. All rights of any nature whatsoever reserved.
format Artículo (Article)
author Arboleda G.
Waters C.
Gibson R.M.
author_facet Arboleda G.
Waters C.
Gibson R.M.
author_sort Arboleda G.
title Metabolic activity: A novel indicator of neuronal survival in the murine dopaminergic cell line CAD
title_short Metabolic activity: A novel indicator of neuronal survival in the murine dopaminergic cell line CAD
title_full Metabolic activity: A novel indicator of neuronal survival in the murine dopaminergic cell line CAD
title_fullStr Metabolic activity: A novel indicator of neuronal survival in the murine dopaminergic cell line CAD
title_full_unstemmed Metabolic activity: A novel indicator of neuronal survival in the murine dopaminergic cell line CAD
title_sort metabolic activity: a novel indicator of neuronal survival in the murine dopaminergic cell line cad
publishDate 2005
url https://repository.urosario.edu.co/handle/10336/22406
https://doi.org/10.1385/JMN:27:01:65
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score 12,131701