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Mesenchymal Stem Cell Transplantation Promotes Neurogenesis and Ameliorates Autism Related Behaviors in BTBR Mice / Hadar SEGAL-GAVISH in Autism Research, 9-1 (January 2016)
[article]
Titre : Mesenchymal Stem Cell Transplantation Promotes Neurogenesis and Ameliorates Autism Related Behaviors in BTBR Mice Type de document : Texte imprimé et/ou numérique Auteurs : Hadar SEGAL-GAVISH, Auteur ; Golan KARVAT, Auteur ; Noy BARAK, Auteur ; Ran BARZILAY, Auteur ; Javier GANZ, Auteur ; Liat EDRY, Auteur ; Israel AHARONY, Auteur ; Daniel OFFEN, Auteur ; Tali KIMCHI, Auteur Article en page(s) : p.17-32 Langues : Anglais (eng) Mots-clés : BTBR animal model MSC BDNF neurogenesis Index. décimale : PER Périodiques Résumé : Autism spectrum disorders (ASD) are characterized by social communication deficits, cognitive rigidity, and repetitive stereotyped behaviors. Mesenchymal stem cells (MSC) have a paracrine regenerative effect, and were speculated to be a potential therapy for ASD. The BTBR inbred mouse strain is a commonly used model of ASD as it demonstrates robust behavioral deficits consistent with the diagnostic criteria for ASD. BTBR mice also exhibit decreased brain-derived neurotrophic factor (BDNF) signaling and reduced hippocampal neurogenesis. In the current study, we evaluated the behavioral and molecular effects of intracerebroventricular MSC transplantation in BTBR mice. Transplantation of MSC resulted in a reduction of stereotypical behaviors, a decrease in cognitive rigidity and an improvement in social behavior. Tissue analysis revealed elevated BDNF protein levels in the hippocampus accompanied by increased hippocampal neurogenesis in the MSC-transplanted mice compared with sham treated mice. This might indicate a possible mechanism underpinning the behavioral improvement. Our study suggests a novel therapeutic approach which may be translatable to ASD patients in the future. En ligne : http://dx.doi.org/10.1002/aur.1530 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=282
in Autism Research > 9-1 (January 2016) . - p.17-32[article] Mesenchymal Stem Cell Transplantation Promotes Neurogenesis and Ameliorates Autism Related Behaviors in BTBR Mice [Texte imprimé et/ou numérique] / Hadar SEGAL-GAVISH, Auteur ; Golan KARVAT, Auteur ; Noy BARAK, Auteur ; Ran BARZILAY, Auteur ; Javier GANZ, Auteur ; Liat EDRY, Auteur ; Israel AHARONY, Auteur ; Daniel OFFEN, Auteur ; Tali KIMCHI, Auteur . - p.17-32.
Langues : Anglais (eng)
in Autism Research > 9-1 (January 2016) . - p.17-32
Mots-clés : BTBR animal model MSC BDNF neurogenesis Index. décimale : PER Périodiques Résumé : Autism spectrum disorders (ASD) are characterized by social communication deficits, cognitive rigidity, and repetitive stereotyped behaviors. Mesenchymal stem cells (MSC) have a paracrine regenerative effect, and were speculated to be a potential therapy for ASD. The BTBR inbred mouse strain is a commonly used model of ASD as it demonstrates robust behavioral deficits consistent with the diagnostic criteria for ASD. BTBR mice also exhibit decreased brain-derived neurotrophic factor (BDNF) signaling and reduced hippocampal neurogenesis. In the current study, we evaluated the behavioral and molecular effects of intracerebroventricular MSC transplantation in BTBR mice. Transplantation of MSC resulted in a reduction of stereotypical behaviors, a decrease in cognitive rigidity and an improvement in social behavior. Tissue analysis revealed elevated BDNF protein levels in the hippocampus accompanied by increased hippocampal neurogenesis in the MSC-transplanted mice compared with sham treated mice. This might indicate a possible mechanism underpinning the behavioral improvement. Our study suggests a novel therapeutic approach which may be translatable to ASD patients in the future. En ligne : http://dx.doi.org/10.1002/aur.1530 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=282 Role of miR-146a in neural stem cell differentiation and neural lineage determination: relevance for neurodevelopmental disorders / L. S. NGUYEN in Molecular Autism, 9 (2018)
[article]
Titre : Role of miR-146a in neural stem cell differentiation and neural lineage determination: relevance for neurodevelopmental disorders Type de document : Texte imprimé et/ou numérique Auteurs : L. S. NGUYEN, Auteur ; J. FREGEAC, Auteur ; C. BOLE-FEYSOT, Auteur ; N. CAGNARD, Auteur ; A. IYER, Auteur ; J. ANINK, Auteur ; E. ARONICA, Auteur ; O. ALIBEU, Auteur ; P. NITSCHKE, Auteur ; L. COLLEAUX, Auteur Article en page(s) : 38p. Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/genetics/metabolism Cell Line Cell Lineage Child Female Humans Male MicroRNAs/genetics/metabolism Neural Stem Cells/cytology/metabolism Neurogenesis Temporal Lobe/cytology/metabolism Up-Regulation Autism spectrum disorders Human neural stem cell Transcriptome microRNA Index. décimale : PER Périodiques Résumé : Background: MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression at the post-transcriptional level. miRNAs have emerged as important modulators of brain development and neuronal function and are implicated in several neurological diseases. Previous studies found miR-146a upregulation is the most common miRNA deregulation event in neurodevelopmental disorders such as autism spectrum disorder (ASD), epilepsy, and intellectual disability (ID). Yet, how miR-146a upregulation affects the developing fetal brain remains unclear. Methods: We analyzed the expression of miR-146a in the temporal lobe of ASD children using Taqman assay. To assess the role of miR-146a in early brain development, we generated and characterized stably induced H9 human neural stem cell (H9 hNSC) overexpressing miR-146a using various cell and molecular biology techniques. Results: We first showed that miR-146a upregulation occurs early during childhood in the ASD brain. In H9 hNSC, miR-146a overexpression enhances neurite outgrowth and branching and favors differentiation into neuronal like cells. Expression analyses revealed that 10% of the transcriptome was deregulated and organized into two modules critical for cell cycle control and neuronal differentiation. Twenty known or predicted targets of miR-146a were significantly deregulated in the modules, acting as potential drivers. The two modules also display distinct transcription profiles during human brain development, affecting regions relevant for ASD including the neocortex, amygdala, and hippocampus. Cell type analyses indicate markers for pyramidal, and interneurons are highly enriched in the deregulated gene list. Up to 40% of known markers of newly defined neuronal lineages were deregulated, suggesting that miR-146a could participate also in the acquisition of neuronal identities. Conclusion: Our results demonstrate the dynamic roles of miR-146a in early neuronal development and provide new insight into the molecular events that link miR-146a overexpression to impaired neurodevelopment. This, in turn, may yield new therapeutic targets and strategies. En ligne : https://dx.doi.org/10.1186/s13229-018-0219-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371
in Molecular Autism > 9 (2018) . - 38p.[article] Role of miR-146a in neural stem cell differentiation and neural lineage determination: relevance for neurodevelopmental disorders [Texte imprimé et/ou numérique] / L. S. NGUYEN, Auteur ; J. FREGEAC, Auteur ; C. BOLE-FEYSOT, Auteur ; N. CAGNARD, Auteur ; A. IYER, Auteur ; J. ANINK, Auteur ; E. ARONICA, Auteur ; O. ALIBEU, Auteur ; P. NITSCHKE, Auteur ; L. COLLEAUX, Auteur . - 38p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 38p.
Mots-clés : Autism Spectrum Disorder/genetics/metabolism Cell Line Cell Lineage Child Female Humans Male MicroRNAs/genetics/metabolism Neural Stem Cells/cytology/metabolism Neurogenesis Temporal Lobe/cytology/metabolism Up-Regulation Autism spectrum disorders Human neural stem cell Transcriptome microRNA Index. décimale : PER Périodiques Résumé : Background: MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression at the post-transcriptional level. miRNAs have emerged as important modulators of brain development and neuronal function and are implicated in several neurological diseases. Previous studies found miR-146a upregulation is the most common miRNA deregulation event in neurodevelopmental disorders such as autism spectrum disorder (ASD), epilepsy, and intellectual disability (ID). Yet, how miR-146a upregulation affects the developing fetal brain remains unclear. Methods: We analyzed the expression of miR-146a in the temporal lobe of ASD children using Taqman assay. To assess the role of miR-146a in early brain development, we generated and characterized stably induced H9 human neural stem cell (H9 hNSC) overexpressing miR-146a using various cell and molecular biology techniques. Results: We first showed that miR-146a upregulation occurs early during childhood in the ASD brain. In H9 hNSC, miR-146a overexpression enhances neurite outgrowth and branching and favors differentiation into neuronal like cells. Expression analyses revealed that 10% of the transcriptome was deregulated and organized into two modules critical for cell cycle control and neuronal differentiation. Twenty known or predicted targets of miR-146a were significantly deregulated in the modules, acting as potential drivers. The two modules also display distinct transcription profiles during human brain development, affecting regions relevant for ASD including the neocortex, amygdala, and hippocampus. Cell type analyses indicate markers for pyramidal, and interneurons are highly enriched in the deregulated gene list. Up to 40% of known markers of newly defined neuronal lineages were deregulated, suggesting that miR-146a could participate also in the acquisition of neuronal identities. Conclusion: Our results demonstrate the dynamic roles of miR-146a in early neuronal development and provide new insight into the molecular events that link miR-146a overexpression to impaired neurodevelopment. This, in turn, may yield new therapeutic targets and strategies. En ligne : https://dx.doi.org/10.1186/s13229-018-0219-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371 Wnt signaling networks in autism spectrum disorder and intellectual disability / V. KWAN in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)
[article]
Titre : Wnt signaling networks in autism spectrum disorder and intellectual disability Type de document : Texte imprimé et/ou numérique Auteurs : V. KWAN, Auteur ; B. K. UNDA, Auteur ; K. K. SINGH, Auteur Article en page(s) : p.45 Langues : Anglais (eng) Mots-clés : Asd Autism spectrum disorders Gsk3 Mutations Neurodevelopment Neurogenesis Neuronal migration Neurotransmission Plasticity Signaling Synapse Wnt signaling Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic factors play a major role in the risk for neurodevelopmental disorders such as autism spectrum disorders (ASDs) and intellectual disability (ID). The underlying genetic factors have become better understood in recent years due to advancements in next generation sequencing. These studies have uncovered a vast number of genes that are impacted by different types of mutations (e.g., de novo, missense, truncation, copy number variations). ABSTRACT: Given the large volume of genetic data, analyzing each gene on its own is not a feasible approach and will take years to complete, let alone attempt to use the information to develop novel therapeutics. To make sense of independent genomic data, one approach is to determine whether multiple risk genes function in common signaling pathways that identify signaling "hubs" where risk genes converge. This approach has led to multiple pathways being implicated, such as synaptic signaling, chromatin remodeling, alternative splicing, and protein translation, among many others. In this review, we analyze recent and historical evidence indicating that multiple risk genes, including genes denoted as high-confidence and likely causal, are part of the Wingless (Wnt signaling) pathway. In the brain, Wnt signaling is an evolutionarily conserved pathway that plays an instrumental role in developing neural circuits and adult brain function. CONCLUSIONS: We will also review evidence that pharmacological therapies and genetic mouse models further identify abnormal Wnt signaling, particularly at the synapse, as being disrupted in ASDs and contributing to disease pathology. En ligne : http://dx.doi.org/10.1186/s11689-016-9176-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=349
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.45[article] Wnt signaling networks in autism spectrum disorder and intellectual disability [Texte imprimé et/ou numérique] / V. KWAN, Auteur ; B. K. UNDA, Auteur ; K. K. SINGH, Auteur . - p.45.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.45
Mots-clés : Asd Autism spectrum disorders Gsk3 Mutations Neurodevelopment Neurogenesis Neuronal migration Neurotransmission Plasticity Signaling Synapse Wnt signaling Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic factors play a major role in the risk for neurodevelopmental disorders such as autism spectrum disorders (ASDs) and intellectual disability (ID). The underlying genetic factors have become better understood in recent years due to advancements in next generation sequencing. These studies have uncovered a vast number of genes that are impacted by different types of mutations (e.g., de novo, missense, truncation, copy number variations). ABSTRACT: Given the large volume of genetic data, analyzing each gene on its own is not a feasible approach and will take years to complete, let alone attempt to use the information to develop novel therapeutics. To make sense of independent genomic data, one approach is to determine whether multiple risk genes function in common signaling pathways that identify signaling "hubs" where risk genes converge. This approach has led to multiple pathways being implicated, such as synaptic signaling, chromatin remodeling, alternative splicing, and protein translation, among many others. In this review, we analyze recent and historical evidence indicating that multiple risk genes, including genes denoted as high-confidence and likely causal, are part of the Wingless (Wnt signaling) pathway. In the brain, Wnt signaling is an evolutionarily conserved pathway that plays an instrumental role in developing neural circuits and adult brain function. CONCLUSIONS: We will also review evidence that pharmacological therapies and genetic mouse models further identify abnormal Wnt signaling, particularly at the synapse, as being disrupted in ASDs and contributing to disease pathology. En ligne : http://dx.doi.org/10.1186/s11689-016-9176-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=349