Genes involved in the balance between neuronal survival and death during inflammation

Glucocorticoids are potent regulators of the innate immune response, and alteration in this inhibitory feedback has detrimental consequences for the neural tissue. This study profiled and investigated functionally candidate genes mediating this switch between cell survival and death during an acute...

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Autor principal:	Chernomoretz, Ariel
Publicado:	2007
Materias:	ceruloplasmin glucocorticoid glucocorticoid receptor lipopolysaccharide oligonucleotide iron animal cell animal experiment animal model article bacterial meningitis cell survival central nervous system disease controlled study corpus striatum degenerative disease demyelination endothelium gene expression regulation gene function gene identification genetic transcription immunopathogenesis innate immunity iron metabolism microarray analysis microglia molecular mechanics mouse nerve cell necrosis neurodegeneration with brain iron accumulation neuroprotection nonhuman receptor blocking signal transduction animal chemically induced disorder demyelinating disease DNA microarray genetics inflammation metabolism methodology mouse mutant nerve cell pathology Mus Animals Cell Survival Ceruloplasmin Demyelinating Diseases Glucocorticoids Inflammation Iron Lipopolysaccharides Mice Mice, Knockout Microarray Analysis Neurons Oligonucleotide Array Sequence Analysis
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19326203_v2_n3_p_Glezer http://hdl.handle.net/20.500.12110/paper_19326203_v2_n3_p_Glezer
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_19326203_v2_n3_p_Glezer
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spelling	paper:paper_19326203_v2_n3_p_Glezer2023-06-08T16:30:50Z Genes involved in the balance between neuronal survival and death during inflammation Chernomoretz, Ariel ceruloplasmin glucocorticoid glucocorticoid receptor lipopolysaccharide oligonucleotide ceruloplasmin glucocorticoid iron lipopolysaccharide animal cell animal experiment animal model article bacterial meningitis cell survival central nervous system disease controlled study corpus striatum degenerative disease demyelination endothelium gene expression regulation gene function gene identification genetic transcription immunopathogenesis innate immunity iron metabolism microarray analysis microglia molecular mechanics mouse nerve cell necrosis neurodegeneration with brain iron accumulation neuroprotection nonhuman receptor blocking signal transduction animal cell survival chemically induced disorder demyelinating disease DNA microarray genetics inflammation metabolism methodology mouse mutant nerve cell pathology Mus Animals Cell Survival Ceruloplasmin Demyelinating Diseases Glucocorticoids Inflammation Iron Lipopolysaccharides Mice Mice, Knockout Microarray Analysis Neurons Oligonucleotide Array Sequence Analysis Glucocorticoids are potent regulators of the innate immune response, and alteration in this inhibitory feedback has detrimental consequences for the neural tissue. This study profiled and investigated functionally candidate genes mediating this switch between cell survival and death during an acute inflammatory reaction subsequent to the absence of glucocorticoid signaling. Oligonucleotide microarray analysis revealed that following lipopolysaccharide (LPS) intracerebral administration at striatum level, more modulated genes presented transcription impairment than exacerbation upon glucocorticoid receptor blockage. Among impaired genes we identified ceruloplasmin (Cp), which plays a key role in iron metabolism and is implicated in a neurodegenative disease. Microglial and endothelial induction of Cp is a natural neuroprotective mechanism during inflammation, because Cp-deficient mice exhibited increased iron accumulation and demyelination when exposed to LPS and neurovascular reactivity to pneumococcal meningitis. This study has identified genes that can play a critical role in programming the innate immune response, helping to clarify the mechanisms leading to protection or damage during inflammatory conditions in the CNS. © 2007 Glezer et al. Fil:Chernomoretz, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2007 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19326203_v2_n3_p_Glezer http://hdl.handle.net/20.500.12110/paper_19326203_v2_n3_p_Glezer
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	ceruloplasmin glucocorticoid glucocorticoid receptor lipopolysaccharide oligonucleotide ceruloplasmin glucocorticoid iron lipopolysaccharide animal cell animal experiment animal model article bacterial meningitis cell survival central nervous system disease controlled study corpus striatum degenerative disease demyelination endothelium gene expression regulation gene function gene identification genetic transcription immunopathogenesis innate immunity iron metabolism microarray analysis microglia molecular mechanics mouse nerve cell necrosis neurodegeneration with brain iron accumulation neuroprotection nonhuman receptor blocking signal transduction animal cell survival chemically induced disorder demyelinating disease DNA microarray genetics inflammation metabolism methodology mouse mutant nerve cell pathology Mus Animals Cell Survival Ceruloplasmin Demyelinating Diseases Glucocorticoids Inflammation Iron Lipopolysaccharides Mice Mice, Knockout Microarray Analysis Neurons Oligonucleotide Array Sequence Analysis
spellingShingle	ceruloplasmin glucocorticoid glucocorticoid receptor lipopolysaccharide oligonucleotide ceruloplasmin glucocorticoid iron lipopolysaccharide animal cell animal experiment animal model article bacterial meningitis cell survival central nervous system disease controlled study corpus striatum degenerative disease demyelination endothelium gene expression regulation gene function gene identification genetic transcription immunopathogenesis innate immunity iron metabolism microarray analysis microglia molecular mechanics mouse nerve cell necrosis neurodegeneration with brain iron accumulation neuroprotection nonhuman receptor blocking signal transduction animal cell survival chemically induced disorder demyelinating disease DNA microarray genetics inflammation metabolism methodology mouse mutant nerve cell pathology Mus Animals Cell Survival Ceruloplasmin Demyelinating Diseases Glucocorticoids Inflammation Iron Lipopolysaccharides Mice Mice, Knockout Microarray Analysis Neurons Oligonucleotide Array Sequence Analysis Chernomoretz, Ariel Genes involved in the balance between neuronal survival and death during inflammation
topic_facet	ceruloplasmin glucocorticoid glucocorticoid receptor lipopolysaccharide oligonucleotide ceruloplasmin glucocorticoid iron lipopolysaccharide animal cell animal experiment animal model article bacterial meningitis cell survival central nervous system disease controlled study corpus striatum degenerative disease demyelination endothelium gene expression regulation gene function gene identification genetic transcription immunopathogenesis innate immunity iron metabolism microarray analysis microglia molecular mechanics mouse nerve cell necrosis neurodegeneration with brain iron accumulation neuroprotection nonhuman receptor blocking signal transduction animal cell survival chemically induced disorder demyelinating disease DNA microarray genetics inflammation metabolism methodology mouse mutant nerve cell pathology Mus Animals Cell Survival Ceruloplasmin Demyelinating Diseases Glucocorticoids Inflammation Iron Lipopolysaccharides Mice Mice, Knockout Microarray Analysis Neurons Oligonucleotide Array Sequence Analysis
description	Glucocorticoids are potent regulators of the innate immune response, and alteration in this inhibitory feedback has detrimental consequences for the neural tissue. This study profiled and investigated functionally candidate genes mediating this switch between cell survival and death during an acute inflammatory reaction subsequent to the absence of glucocorticoid signaling. Oligonucleotide microarray analysis revealed that following lipopolysaccharide (LPS) intracerebral administration at striatum level, more modulated genes presented transcription impairment than exacerbation upon glucocorticoid receptor blockage. Among impaired genes we identified ceruloplasmin (Cp), which plays a key role in iron metabolism and is implicated in a neurodegenative disease. Microglial and endothelial induction of Cp is a natural neuroprotective mechanism during inflammation, because Cp-deficient mice exhibited increased iron accumulation and demyelination when exposed to LPS and neurovascular reactivity to pneumococcal meningitis. This study has identified genes that can play a critical role in programming the innate immune response, helping to clarify the mechanisms leading to protection or damage during inflammatory conditions in the CNS. © 2007 Glezer et al.
author	Chernomoretz, Ariel
author_facet	Chernomoretz, Ariel
author_sort	Chernomoretz, Ariel
title	Genes involved in the balance between neuronal survival and death during inflammation
title_short	Genes involved in the balance between neuronal survival and death during inflammation
title_full	Genes involved in the balance between neuronal survival and death during inflammation
title_fullStr	Genes involved in the balance between neuronal survival and death during inflammation
title_full_unstemmed	Genes involved in the balance between neuronal survival and death during inflammation
title_sort	genes involved in the balance between neuronal survival and death during inflammation
publishDate	2007
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19326203_v2_n3_p_Glezer http://hdl.handle.net/20.500.12110/paper_19326203_v2_n3_p_Glezer
work_keys_str_mv	AT chernomoretzariel genesinvolvedinthebalancebetweenneuronalsurvivalanddeathduringinflammation
_version_	1768544059251490816

Genes involved in the balance between neuronal survival and death during inflammation

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