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Transcriptome analysis of microglia in a mouse model of Rett syndrome: differential expression of genes associated with microglia/macrophage activation and cellular stress / D. ZHAO in Molecular Autism, 8 (2017)
[article]
Titre : Transcriptome analysis of microglia in a mouse model of Rett syndrome: differential expression of genes associated with microglia/macrophage activation and cellular stress Type de document : Texte imprimé et/ou numérique Auteurs : D. ZHAO, Auteur ; R. MOKHTARI, Auteur ; E. PEDROSA, Auteur ; R. BIRNBAUM, Auteur ; D. ZHENG, Auteur ; H. M. LACHMAN, Auteur Article en page(s) : 17p. Langues : Anglais (eng) Mots-clés : Animals Disease Models, Animal Female Gene Expression Profiling/*methods Gene Expression Regulation Heat-Shock Proteins/genetics Humans Macrophage Activation Macrophages/*cytology Methyl-CpG-Binding Protein 2/*deficiency Mice Microglia/*metabolism Mutation Oxidative Stress Rett Syndrome/*genetics Sequence Analysis, RNA/*methods *Autism *Heat shock *Innate immune system *M1 activation *M2 activation *Microglia *Rett syndrome *Schizophrenia Index. décimale : PER Périodiques Résumé : BACKGROUND: Rett syndrome (RTT) is a severe, neurodevelopmental disorder primarily affecting girls, characterized by progressive loss of cognitive, social, and motor skills after a relatively brief period of typical development. It is usually due to de novo loss of function mutations in the X-linked gene, MeCP2, which codes for the gene expression and chromatin regulator, methyl-CpG binding protein 2. Although the behavioral phenotype appears to be primarily due to neuronal Mecp2 deficiency in mice, other cell types, including astrocytes and oligodendrocytes, also appear to contribute to some aspects of the RTT phenotype. In addition, microglia may also play a role. However, the effect of Mecp2 deficiency in microglia on RTT pathogenesis is controversial. METHODS: In the current study, we applied whole transcriptome analysis using RNA-seq to gain insight into molecular pathways in microglia that might be dysregulated during the transition, in female mice heterozygous for an Mecp2-null allele (Mecp2(+/-); Het), from the pre-phenotypic (5 weeks) to the phenotypic phases (24 weeks). RESULTS: We found a significant overlap in differentially expressed genes (DEGs) with genes involved in regulating the extracellular matrix, and those that are activated or inhibited when macrophages and microglia are stimulated towards the M1 and M2 activation states. However, the M1- and M2-associated genes were different in the 5- and 24-week samples. In addition, a substantial decrease in the expression of nine members of the heat shock protein (HSP) family was found in the 5-week samples, but not at 24 weeks. CONCLUSIONS: These findings suggest that microglia from pre-phenotypic and phenotypic female mice are activated in a manner different from controls and that pre-phenotypic female mice may have alterations in their capacity to response to heat stress and other stressors that function through the HSP pathway. En ligne : http://dx.doi.org/10.1186/s13229-017-0134-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331
in Molecular Autism > 8 (2017) . - 17p.[article] Transcriptome analysis of microglia in a mouse model of Rett syndrome: differential expression of genes associated with microglia/macrophage activation and cellular stress [Texte imprimé et/ou numérique] / D. ZHAO, Auteur ; R. MOKHTARI, Auteur ; E. PEDROSA, Auteur ; R. BIRNBAUM, Auteur ; D. ZHENG, Auteur ; H. M. LACHMAN, Auteur . - 17p.
Langues : Anglais (eng)
in Molecular Autism > 8 (2017) . - 17p.
Mots-clés : Animals Disease Models, Animal Female Gene Expression Profiling/*methods Gene Expression Regulation Heat-Shock Proteins/genetics Humans Macrophage Activation Macrophages/*cytology Methyl-CpG-Binding Protein 2/*deficiency Mice Microglia/*metabolism Mutation Oxidative Stress Rett Syndrome/*genetics Sequence Analysis, RNA/*methods *Autism *Heat shock *Innate immune system *M1 activation *M2 activation *Microglia *Rett syndrome *Schizophrenia Index. décimale : PER Périodiques Résumé : BACKGROUND: Rett syndrome (RTT) is a severe, neurodevelopmental disorder primarily affecting girls, characterized by progressive loss of cognitive, social, and motor skills after a relatively brief period of typical development. It is usually due to de novo loss of function mutations in the X-linked gene, MeCP2, which codes for the gene expression and chromatin regulator, methyl-CpG binding protein 2. Although the behavioral phenotype appears to be primarily due to neuronal Mecp2 deficiency in mice, other cell types, including astrocytes and oligodendrocytes, also appear to contribute to some aspects of the RTT phenotype. In addition, microglia may also play a role. However, the effect of Mecp2 deficiency in microglia on RTT pathogenesis is controversial. METHODS: In the current study, we applied whole transcriptome analysis using RNA-seq to gain insight into molecular pathways in microglia that might be dysregulated during the transition, in female mice heterozygous for an Mecp2-null allele (Mecp2(+/-); Het), from the pre-phenotypic (5 weeks) to the phenotypic phases (24 weeks). RESULTS: We found a significant overlap in differentially expressed genes (DEGs) with genes involved in regulating the extracellular matrix, and those that are activated or inhibited when macrophages and microglia are stimulated towards the M1 and M2 activation states. However, the M1- and M2-associated genes were different in the 5- and 24-week samples. In addition, a substantial decrease in the expression of nine members of the heat shock protein (HSP) family was found in the 5-week samples, but not at 24 weeks. CONCLUSIONS: These findings suggest that microglia from pre-phenotypic and phenotypic female mice are activated in a manner different from controls and that pre-phenotypic female mice may have alterations in their capacity to response to heat stress and other stressors that function through the HSP pathway. En ligne : http://dx.doi.org/10.1186/s13229-017-0134-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331 Neuroglia in the autistic brain: evidence from a preclinical model / M. R. BRONZUOLI in Molecular Autism, 9 (2018)
[article]
Titre : Neuroglia in the autistic brain: evidence from a preclinical model Type de document : Texte imprimé et/ou numérique Auteurs : M. R. BRONZUOLI, Auteur ; R. FACCHINETTI, Auteur ; D. INGRASSIA, Auteur ; M. SARVADIO, Auteur ; S. SCHIAVI, Auteur ; L. STEARDO, Auteur ; A. VERKHRATSKY, Auteur ; V. TREZZA, Auteur ; C. SCUDERI, Auteur Article en page(s) : 66 p. Langues : Anglais (eng) Mots-clés : Animals Autistic Disorder/etiology/*pathology/physiopathology Brain/drug effects/*pathology Female Male Neuroglia/drug effects/*pathology Rats Rats, Wistar Stereotyped Behavior Valproic Acid/pharmacology/toxicity Vocalization, Animal *Astrocyte *Autism spectrum disorder *Microglia *Oligodendrocyte *Valproic acid of the Italian Ministry of Health (D.L. 26/2014) and with the European Parliament directive 2010/63/EU.Not applicable.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Index. décimale : PER Périodiques Résumé : Background: Neuroglial cells that provide homeostatic support and form defence of the nervous system contribute to all neurological disorders. We analyzed three major types of neuroglia, astrocytes, oligodendrocytes, and microglia in the brains of an animal model of autism spectrum disorder, in which rats were exposed prenatally to antiepileptic and mood stabilizer drug valproic acid; this model being of acknowledged clinical relevance. Methods: We tested the autistic-like behaviors of valproic acid-prenatally exposed male rats by performing isolation-induced ultrasonic vocalizations, the three-chamber test, and the hole board test. To account for human infancy, adolescence, and adulthood, such tasks were performed at postnatal day 13, postnatal day 35, and postnatal day 90, respectively. After sacrifice, we examined gene and protein expression of specific markers of neuroglia in hippocampus, prefrontal cortex, and cerebellum, these brain regions being associated with autism spectrum disorder pathogenesis. Results: Infant offspring of VPA-exposed dams emitted less ultrasonic vocalizations when isolated from their mothers and siblings and, in adolescence and adulthood, they showed altered sociability in the three chamber test and increased stereotypic behavior in the hole board test. Molecular analyses indicate that prenatal valproic acid exposure affects all types of neuroglia, mainly causing transcriptional modifications. The most prominent changes occur in prefrontal cortex and in the hippocampus of autistic-like animals; these changes are particularly evident during infancy and adolescence, while they appear to be mitigated in adulthood. Conclusions: Neuroglial pathological phenotype in autism spectrum disorder rat model appears to be rather mild with little signs of widespread and chronic neuroinflammation. En ligne : https://dx.doi.org/10.1186/s13229-018-0254-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=389
in Molecular Autism > 9 (2018) . - 66 p.[article] Neuroglia in the autistic brain: evidence from a preclinical model [Texte imprimé et/ou numérique] / M. R. BRONZUOLI, Auteur ; R. FACCHINETTI, Auteur ; D. INGRASSIA, Auteur ; M. SARVADIO, Auteur ; S. SCHIAVI, Auteur ; L. STEARDO, Auteur ; A. VERKHRATSKY, Auteur ; V. TREZZA, Auteur ; C. SCUDERI, Auteur . - 66 p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 66 p.
Mots-clés : Animals Autistic Disorder/etiology/*pathology/physiopathology Brain/drug effects/*pathology Female Male Neuroglia/drug effects/*pathology Rats Rats, Wistar Stereotyped Behavior Valproic Acid/pharmacology/toxicity Vocalization, Animal *Astrocyte *Autism spectrum disorder *Microglia *Oligodendrocyte *Valproic acid of the Italian Ministry of Health (D.L. 26/2014) and with the European Parliament directive 2010/63/EU.Not applicable.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Index. décimale : PER Périodiques Résumé : Background: Neuroglial cells that provide homeostatic support and form defence of the nervous system contribute to all neurological disorders. We analyzed three major types of neuroglia, astrocytes, oligodendrocytes, and microglia in the brains of an animal model of autism spectrum disorder, in which rats were exposed prenatally to antiepileptic and mood stabilizer drug valproic acid; this model being of acknowledged clinical relevance. Methods: We tested the autistic-like behaviors of valproic acid-prenatally exposed male rats by performing isolation-induced ultrasonic vocalizations, the three-chamber test, and the hole board test. To account for human infancy, adolescence, and adulthood, such tasks were performed at postnatal day 13, postnatal day 35, and postnatal day 90, respectively. After sacrifice, we examined gene and protein expression of specific markers of neuroglia in hippocampus, prefrontal cortex, and cerebellum, these brain regions being associated with autism spectrum disorder pathogenesis. Results: Infant offspring of VPA-exposed dams emitted less ultrasonic vocalizations when isolated from their mothers and siblings and, in adolescence and adulthood, they showed altered sociability in the three chamber test and increased stereotypic behavior in the hole board test. Molecular analyses indicate that prenatal valproic acid exposure affects all types of neuroglia, mainly causing transcriptional modifications. The most prominent changes occur in prefrontal cortex and in the hippocampus of autistic-like animals; these changes are particularly evident during infancy and adolescence, while they appear to be mitigated in adulthood. Conclusions: Neuroglial pathological phenotype in autism spectrum disorder rat model appears to be rather mild with little signs of widespread and chronic neuroinflammation. En ligne : https://dx.doi.org/10.1186/s13229-018-0254-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=389