Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA214942 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In the largest published genome-wide association study (GWAS) of schizophrenia to date (PGC1), the most significant association (P = 1.6 X 10-11) was observed at an intronic variant (rs1625579) within the MIR137 host gene (MIR137HG). In this study we have performed genome-wide RNA profiling of a human foetal neural progenitor cell line following miR-137 manipulation, in order to identify gene expression changes through which genetic variation at the MIR137HG locus could confer susceptibility to schizophrenia. Total RNA extracted from human neural progenitor cells manipulated with either mir137 inhibitor or mimic. 4 replicates per group. Genome wide transcript levels were then measured using gene expression microarrays.
2014-02-10 | E-GEOD-49793 | biostudies-arrayexpress
Project description:In the largest published genome-wide association study (GWAS) of schizophrenia to date (PGC1), the most significant association (P = 1.6 X 10-11) was observed at an intronic variant (rs1625579) within the MIR137 host gene (MIR137HG). In this study we have performed genome-wide RNA profiling of a human foetal neural progenitor cell line following miR-137 manipulation, in order to identify gene expression changes through which genetic variation at the MIR137HG locus could confer susceptibility to schizophrenia.
2014-02-10 | GSE49793 | GEO
Project description:Recent genetic evidence has revealed microRNA-137 (miR-137) as a risk gene in schizophrenia and autism spectrum disorder (ASD), and the following cellular studies have demonstrated the importance of miR-137 in regulating neurogenesis. We have generated miR-137 knockout mice which display behaviors that resemble some symptoms of these two diseases. To investigate the underlying molecular mechanism, we performed comprehensive analyses of the entire RNA and protein molecules of the miR-137 mouse brains. The dataset uploaded here is the raw data of the mass spectrometry-based whole proteome analysis of the six miR-137 mouse brains: wild-type, heterozygous (miR-137+/–) and homozygous (miR-137–/–) from two different litters. The tandem mass tag (TMT) methodology was employed in this proteomics analysis for the quantitation. The sample channels are: 128C (miR-137+/+, litter 1), 129N (miR-137+/–, litter 1), 129C (miR-137–/–, litter 1), 130N (miR-137+/+, litter 2), 130C (miR-137+/–, litter 2), and 131N (miR-137–/–, litter 2).
2018-10-17 | PXD003874 | Pride
Project description:Genetic analyses have linked microRNA-137 (MIR137) to neuropsychiatric disorders, including schizophrenia and autism spectrum disorder. miR-137 plays important roles in neurogenesis and neuronal maturation, but the impact of miR-137 loss-of-function in vivo remains unclear. Here we show the complete loss of miR-137 in the mouse germline (gKO) or nervous system (cKO) leads to postnatal lethality, while heterozygous gKO and cKO mice remain viable. Partial loss of miR-137 in heterozygous cKO mice results in dysregulated synaptic plasticity, repetitive behavior, and impaired learning and social behavior. Transcriptomic and proteomic analyses revealed that the miR-137 mRNA target, phosphodiesterase 10a (Pde10a), is elevated in heterozygous knockout mice. Treatment with the Pde10a inhibitor papaverine or knockdown of Pde10a ameliorates the deficits observed in the heterozygous cKO mice. Collectively, our results suggest that MIR137 plays essential roles in postnatal neurodevelopment and that dysregulation of miR-137 potentially contributes to neuropsychiatric disorders in humans.
2018-10-09 | GSE79661 | GEO
Project description:Drug addiction is a major public health issue that is characterised by continued drug use despite negative consequences. However, the molecular and cellular mechanisms that underlie this behaviour are not well understood. In this study we investigated the role of miR-137, a microRNA that has been previously shown to control the expression of genes necessary for neuronal development and synapse maturation, with common variants in the MIR137 gene linked to a higher risk of schizophrenia. Previously, we revealed that miR-137 expression in cocaine-trained animals exhibited spatial and temporal variability in the dorsal striatum (DS). Building upon this observation, we hypothesised that augmenting miR-137 function in the DS would impact drug-seeking behavior under punishment conditions by modulating molecular targets involved in synaptic plasticity. Male Sprague-Dawley rats were trained to self-administer cocaine and then randomly assigned to receive either lentiviral-mediated overexpression of hsa-miR-137 (miR-137OE) or an empty pCDH-vector (pCDH-EV) control in the dorsomedial striatum (DMS). Once stable cocaine self-administration was achieved, drug-taking was assessed under conditions in which lever presses were associated with a 0.25 probability of foot shock (0.5 mA). During five days of testing, pCDH-EV control animals showed a significant reduction in responding for cocaine, whereas miR-137OE animals displayed greater resistance to the suppression of cocaine responding across foot shock sessions compared to controls. RNA-sequencing analysis of striatal tissue from miR-137OE animals revealed significant enrichment of genes involved in synaptic plasticity and astrocyte signalling compared to control animals. Taken together, these findings provide insight into the mechanisms underlying addiction risk and and contribute to a better understanding of the neural substrates involved in these disorders.
2024-12-31 | GSE246334 | GEO
Project description:A hallmark of cortical evolution is the high dynamic subventricular zone (SVZ) expansion, where basal progenitors (BPs) amplify and neuronal transcriptional programs unfold. How non-coding molecular factors such as microRNAs influence these developmental trajectories and regulate the acquisition of cortical type identities is largely unknown. Here we demonstrate that miR-137 and miR-122 regulate the positioning and identity features of superficial layer cortical neurons by acting at distinct steps of their developmental trajectories. MiR-137 sustains basal progenitor amplification by reverting their neurogenic commitment and inducing high proliferative state upregulating Cd63 and inhibiting Myt1l. Cd63 is an extra-cellular matrix (ECM) receptor which interacts with b3- and 1-integrin pathways to promote proliferation, while Myt1l is a transcription factor that promotes and sustains neuronal fate. The BPs amplification by miR-137 is converted in the promotion of intracortical projecting neuron (ICPN) identity and L2/3 expansion. As opposed to miR-137, miR-122 acts postmitotically, affecting the bioelectrical properties, the calcium and cytoskeleton dynamics of newborn neurons as well as their transcriptional program, leading to a persistent molecular immaturity across time. Overall, these findings reveal that miR-137 and miR-122 are key regulators of the developmental trajectory of cortical neurons across evolution.
2022-03-09 | GSE159596 | GEO
Project description:MicroRNAs have been implicated in the pathology not only of cancer, but also of psychiatric diseases, such as bipolar disorder and schizophrenia. As several psychiatric disorders share the same risk genes, we hypothesized that this microRNA could also be associated with attention-deficit/hyperactivity disorder (ADHD) and that this association to psychiatric disorders might be due to the variable number of tandem repeats (VNTR) polymorphism within the internal miR-137 (Imir137) promoter (PMID 18316599; PMID 25154622). To further understand the role of the microRNA 137 in the brain a knock-down of miR-137 expression in SH-SY5Y neuroblastoma cells was performed followed by expression analysis using a microarray.
2018-12-01 | GSE66433 | GEO
Project description:Transcriptional consequences of DISC1 knockdown in human neural progenitor cells
| PRJNA152283 | ENA
Project description:miR-137 plays critical roles in the nervous system and tumor development. An increase in its expression is required for neuronal differentiation while its reduction is implicated in gliomagenesis. To evaluate the potential of miR-137 in glioblastoma therapy, we conducted genome-wide target mapping in glioblastoma cells by measuring levels of associations between PABP and mRNAs in cells transfected with miR-137 mimics vs. controls via RIPSeq. Impact on mRNA levels was also measured by RNASeq. By combining the results of both experimental approaches, 1468 genes were determined to be negatively impacted by miR-137; among them, 595 (40%) contain miR-137 predicted sites. The most relevant targets include oncogenic proteins and players in neurogenesis like c-KIT, YBX1, AKT2, CDC42, CDK6 and TGFβ2. Interestingly, we observed that several identified miR-137 targets are also predicted to be regulated by miR-124, miR-128 and miR-7, which are equally implicated in neuronal differentiation and gliomagenesis. We suggest that the concomitant increase of these four miRNAs in neuronal stem cells or their repression in tumor cells could produce a robust regulatory effect with major consequences to neuronal differentiation and tumorigenesis. Identification of genes affected by miR137 transfection via RIP-Seq and RNA-Seq in U251 and U343 cells
2014-02-11 | E-GEOD-53220 | biostudies-arrayexpress
Project description:miR-137 plays critical roles in the nervous system and tumor development. An increase in its expression is required for neuronal differentiation while its reduction is implicated in gliomagenesis. To evaluate the potential of miR-137 in glioblastoma therapy, we conducted genome-wide target mapping in glioblastoma cells by measuring levels of associations between PABP and mRNAs in cells transfected with miR-137 mimics vs. controls via RIPSeq. Impact on mRNA levels was also measured by RNASeq. By combining the results of both experimental approaches, 1468 genes were determined to be negatively impacted by miR-137; among them, 595 (40%) contain miR-137 predicted sites. The most relevant targets include oncogenic proteins and players in neurogenesis like c-KIT, YBX1, AKT2, CDC42, CDK6 and TGFβ2. Interestingly, we observed that several identified miR-137 targets are also predicted to be regulated by miR-124, miR-128 and miR-7, which are equally implicated in neuronal differentiation and gliomagenesis. We suggest that the concomitant increase of these four miRNAs in neuronal stem cells or their repression in tumor cells could produce a robust regulatory effect with major consequences to neuronal differentiation and tumorigenesis.
2014-02-11 | GSE53220 | GEO