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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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 |
_version_ |
1740172669875126272 |
score |
12,131701 |