Progressive neurodegeneration and motor disabilities induced by chronic expression of IL-1β in the substantia nigra

The functional role of the long-lasting inflammation found in the substantia nigra (SN) of Parkinson's disease (PD) patients and animal models is unclear. Proinflammatory cytokines such as interleukin-1β (IL-1β) could be involved in mediating neuronal demise. However, it is unknown whether the...

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Autores principales:	Ferrari, C.C., Pott Godoy, M.C., Tarelli, R., Chertoff, M., Depino, A.M., Pitossi, F.J.
Formato:	JOUR
Materias:	Adenovector Akinesia Cytokine Inflammation Microglia Parkinson interleukin 1beta Adenovirus akinesia animal experiment animal model animal tissue article astrocyte cell activation cell death controlled study disease course dopaminergic nerve cell immunohistochemistry inflammatory infiltrate male microglia motor dysfunction nerve degeneration nonhuman pathogenesis pathophysiology priority journal protein expression rat scar formation substantia nigra virus recombinant Adenoviridae Animals Astrocytes Cell Death Cytokines Dopamine Genetic Vectors Glial Fibrillary Acidic Protein Interleukin-1 Macrophage Activation Macrophages Male Motor Activity Movement Disorders Nerve Degeneration Neuroglia Neurons Parkinson Disease, Secondary Rats Rats, Wistar Substantia Nigra
Acceso en línea:	http://hdl.handle.net/20.500.12110/paper_09699961_v24_n1_p183_Ferrari
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

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spelling	todo:paper_09699961_v24_n1_p183_Ferrari2023-10-03T15:55:33Z Progressive neurodegeneration and motor disabilities induced by chronic expression of IL-1β in the substantia nigra Ferrari, C.C. Pott Godoy, M.C. Tarelli, R. Chertoff, M. Depino, A.M. Pitossi, F.J. Adenovector Akinesia Cytokine Inflammation Microglia Parkinson interleukin 1beta Adenovirus akinesia animal experiment animal model animal tissue article astrocyte cell activation cell death controlled study disease course dopaminergic nerve cell immunohistochemistry inflammatory infiltrate male microglia motor dysfunction nerve degeneration nonhuman pathogenesis pathophysiology priority journal protein expression rat scar formation substantia nigra virus recombinant Adenoviridae Animals Astrocytes Cell Death Cytokines Dopamine Genetic Vectors Glial Fibrillary Acidic Protein Interleukin-1 Macrophage Activation Macrophages Male Microglia Motor Activity Movement Disorders Nerve Degeneration Neuroglia Neurons Parkinson Disease, Secondary Rats Rats, Wistar Substantia Nigra The functional role of the long-lasting inflammation found in the substantia nigra (SN) of Parkinson's disease (PD) patients and animal models is unclear. Proinflammatory cytokines such as interleukin-1β (IL-1β) could be involved in mediating neuronal demise. However, it is unknown whether the chronic expression of cytokines such as IL-1β in the SN can alter neuronal vitality. The aim of this study was to investigate the effects of the chronic expression of IL-1β in the adult rat SN using a recombinant adenovirus expressing IL-1β. The chronic expression of IL-1β for 60 days induced dopaminergic cell death in the SN and unilateral akinesia starting only at 21 days post-injection. Microglial cell activation and inflammatory cell infiltrate were associated with dopaminergic cell death and motor disabilities. Astrocytic activation was delayed and associated with scar formation. The chronic expression of a single proinflammatory cytokine as IL-1β in the SN elicited most of the characteristics of PD, including progressive dopaminergic cell death, akinesia and glial activation. Our data suggest that IL-1β per se is able to mediate inflammatory-mediated toxic effects in the SN if its expression is sustained. This model will be helpful to identify possible therapeutic targets related to inflammation-derived neurodegeneration in the SN. © 2006 Elsevier Inc. All rights reserved. Fil:Ferrari, C.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Pott Godoy, M.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Tarelli, R. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Chertoff, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Depino, A.M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_09699961_v24_n1_p183_Ferrari
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	Adenovector Akinesia Cytokine Inflammation Microglia Parkinson interleukin 1beta Adenovirus akinesia animal experiment animal model animal tissue article astrocyte cell activation cell death controlled study disease course dopaminergic nerve cell immunohistochemistry inflammatory infiltrate male microglia motor dysfunction nerve degeneration nonhuman pathogenesis pathophysiology priority journal protein expression rat scar formation substantia nigra virus recombinant Adenoviridae Animals Astrocytes Cell Death Cytokines Dopamine Genetic Vectors Glial Fibrillary Acidic Protein Interleukin-1 Macrophage Activation Macrophages Male Microglia Motor Activity Movement Disorders Nerve Degeneration Neuroglia Neurons Parkinson Disease, Secondary Rats Rats, Wistar Substantia Nigra
spellingShingle	Adenovector Akinesia Cytokine Inflammation Microglia Parkinson interleukin 1beta Adenovirus akinesia animal experiment animal model animal tissue article astrocyte cell activation cell death controlled study disease course dopaminergic nerve cell immunohistochemistry inflammatory infiltrate male microglia motor dysfunction nerve degeneration nonhuman pathogenesis pathophysiology priority journal protein expression rat scar formation substantia nigra virus recombinant Adenoviridae Animals Astrocytes Cell Death Cytokines Dopamine Genetic Vectors Glial Fibrillary Acidic Protein Interleukin-1 Macrophage Activation Macrophages Male Microglia Motor Activity Movement Disorders Nerve Degeneration Neuroglia Neurons Parkinson Disease, Secondary Rats Rats, Wistar Substantia Nigra Ferrari, C.C. Pott Godoy, M.C. Tarelli, R. Chertoff, M. Depino, A.M. Pitossi, F.J. Progressive neurodegeneration and motor disabilities induced by chronic expression of IL-1β in the substantia nigra
topic_facet	Adenovector Akinesia Cytokine Inflammation Microglia Parkinson interleukin 1beta Adenovirus akinesia animal experiment animal model animal tissue article astrocyte cell activation cell death controlled study disease course dopaminergic nerve cell immunohistochemistry inflammatory infiltrate male microglia motor dysfunction nerve degeneration nonhuman pathogenesis pathophysiology priority journal protein expression rat scar formation substantia nigra virus recombinant Adenoviridae Animals Astrocytes Cell Death Cytokines Dopamine Genetic Vectors Glial Fibrillary Acidic Protein Interleukin-1 Macrophage Activation Macrophages Male Microglia Motor Activity Movement Disorders Nerve Degeneration Neuroglia Neurons Parkinson Disease, Secondary Rats Rats, Wistar Substantia Nigra
description	The functional role of the long-lasting inflammation found in the substantia nigra (SN) of Parkinson's disease (PD) patients and animal models is unclear. Proinflammatory cytokines such as interleukin-1β (IL-1β) could be involved in mediating neuronal demise. However, it is unknown whether the chronic expression of cytokines such as IL-1β in the SN can alter neuronal vitality. The aim of this study was to investigate the effects of the chronic expression of IL-1β in the adult rat SN using a recombinant adenovirus expressing IL-1β. The chronic expression of IL-1β for 60 days induced dopaminergic cell death in the SN and unilateral akinesia starting only at 21 days post-injection. Microglial cell activation and inflammatory cell infiltrate were associated with dopaminergic cell death and motor disabilities. Astrocytic activation was delayed and associated with scar formation. The chronic expression of a single proinflammatory cytokine as IL-1β in the SN elicited most of the characteristics of PD, including progressive dopaminergic cell death, akinesia and glial activation. Our data suggest that IL-1β per se is able to mediate inflammatory-mediated toxic effects in the SN if its expression is sustained. This model will be helpful to identify possible therapeutic targets related to inflammation-derived neurodegeneration in the SN. © 2006 Elsevier Inc. All rights reserved.
format	JOUR
author	Ferrari, C.C. Pott Godoy, M.C. Tarelli, R. Chertoff, M. Depino, A.M. Pitossi, F.J.
author_facet	Ferrari, C.C. Pott Godoy, M.C. Tarelli, R. Chertoff, M. Depino, A.M. Pitossi, F.J.
author_sort	Ferrari, C.C.
title	Progressive neurodegeneration and motor disabilities induced by chronic expression of IL-1β in the substantia nigra
title_short	Progressive neurodegeneration and motor disabilities induced by chronic expression of IL-1β in the substantia nigra
title_full	Progressive neurodegeneration and motor disabilities induced by chronic expression of IL-1β in the substantia nigra
title_fullStr	Progressive neurodegeneration and motor disabilities induced by chronic expression of IL-1β in the substantia nigra
title_full_unstemmed	Progressive neurodegeneration and motor disabilities induced by chronic expression of IL-1β in the substantia nigra
title_sort	progressive neurodegeneration and motor disabilities induced by chronic expression of il-1β in the substantia nigra
url	http://hdl.handle.net/20.500.12110/paper_09699961_v24_n1_p183_Ferrari
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Progressive neurodegeneration and motor disabilities induced by chronic expression of IL-1β in the substantia nigra

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