Contribution of Age, Brain Region, Mood Disorder Pathology, and Interindividual Factors on the Methylome of Human Microglia
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA790390 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Total of 56 microglia samples from postmortem brain tissue of four different brain regions, medial frontal gyrus (MFG), superior temporal gyrus (STG), subventricular zone (SVZ) and thalamus (THA), of 22 donors, encompassing 1 patient with schizophrenia, 13 patients with mood disorder pathology, and 8 control subjects, were isolated and assayed using a genome-wide methylation array to characterize the DNA methylation landscape of human microglia and the factors that contribute to variations in the microglia methylome
2022-01-31 | GSE191200 | GEO
Project description:Interindividual variation in methylation profiling of human DNA samples were detected using two-tissue screening by MSAM. 0.5ug of DNA was serially digested with SmaI and XmaI followed by an adaptor ligation and adaptor mediated PCR amplification HF (hair follicle) and PBL (Peripheral Blood Leukocyte) DNA samples for 8 different individuals, two-color experiment, interindividual paired comparison (same sex and age)
2010-12-01 | E-GEOD-19823 | biostudies-arrayexpress
Project description:Severe acute respiratory syndrome coronavirus (SARS-CoV) causes lethal disease in humans, with viral E protein promoting the exacerbated inflammatory response. By deep sequencing RNAs from the lungs of infected mice, we have addressed the relevance of small, non-coding RNAs in SARS-CoV pathology. Host microRNAs (miRNAs) expressed during infection by a virulent virus encoding the E protein were significantly enriched for cytokine-mediated inflammatory pathways when compared with attenuated SARS-CoV-∆E, suggesting contribution of miRNAs to E protein-induced inflammation. The discovery of three 18-22 nt small viral RNAs (svRNAs) derived from the nsp3 and N genomic regions of SARS-CoV in mouse lung and cell cultures is also described. Depletion of these svRNAs significantly reduced viral titers and genomic RNA levels, indicating their positive contribution to virus growth. Remarkably, svRNA-N antagomirs significantly reduced in vivo lung pathology and pro-inflammatory cytokine expression, indicating that svRNAs contribute to SARS-CoV pathogenesis and highlighting the potential of these antagomirs as antivirals.
2022-02-04 | GSE84081 | GEO
Project description:We used an unbiased approach to identify differences in gene expression that may account for the high degree of interindividual variability in inflammatory responses to LPS in the normal human population. We measured LPS-induced cytokine production ex vivo in whole blood from 102 healthy human subjects and identified individuals who consistently showed either very high or very low responses to LPS. Comparison of gene expression profiles between the lpshigh and lpslow individuals revealed 80 genes that were differentially expressed in the presence of LPS and 21 genes that were differentially expressed in the absence of LPS (p < 0.005, ANOVA). Expression of a subset of these genes was confirmed using real-time RT-PCR. These data illustrate a novel approach to the identification of factors that determine interindividual variability in innate immune inflammatory responses. Keywords: comparative response
2005-10-22 | GSE3491 | GEO
Project description:Interindividual variation in methylation profiling of human DNA samples were detected using two-tissue screening by MSAM. 0.5ug of DNA was serially digested with SmaI and XmaI followed by an adaptor ligation and adaptor mediated PCR amplification
2010-12-01 | GSE19823 | GEO
Project description:Contribution of host miRNA-223-3p to SARS-CoV-induced lung inflammatory pathology
| PRJNA748712 | ENA
Project description:Abstract Background Neurexins are proteins located in the presynaptic membrane that bind postsynaptic ligands, neuroligins, neurexophilins, and dystrophoglycan. They exert profound effects on neurological function by mediating signalling across synapses and determining synaptic characteristics through the recruitment of additional proteins for synapse formation. Alterations in neurexin-encoding genes cause cognitive disorders such as autism, developmental delay and schizophrenia. The three neurexin genes in the human genome (NRXN1, NRXN2, and NRXN3) each have two different functional promoters, producing a large (alpha) and small (beta) transcript with corresponding proteins. NRXN1 produces hundreds, perhaps thousands, of different transcripts with differential localization in the CNS. Results We report here the identification of an individual (53825) with mild dysmorphia, severe language disorder, mild intellectual disability, attention deficit hyperactivity disorder (ADHD), and a mood disorder. Genomic analysis by Affymetrix 6.0 Gene Chip and FISH (fluorescence in situ hybridization) using probes specific for NRXN1 revealed a hemizygous deletion of approximately 190 Kb, which includes exons 3-5 of NRXN1. This deletion should result in the absence of the vast majority of different NRXN1 alpha transcripts from one of the NRXN1 gene copies, without effecting NRXN1 beta transcription. Copy number analysis of Affymetrix 6.0 SNP arrays was performed according to the manufacturer's directions on DNA extracted from cryopreserved diagnostic bone marrow or peripheral blood samples for pediatric patients. One sample showed partial deletion of NRXN1 alpha; data presented in this Series.
2011-06-24 | E-GEOD-23358 | biostudies-arrayexpress
Project description:The Mood and Methylation Study (MMS)
| PRJNA821589 | ENA
Project description:The Mood and Methylation Study (MMS)
| PRJNA821591 | ENA
Project description:Abstract Background Neurexins are proteins located in the presynaptic membrane that bind postsynaptic ligands, neuroligins, neurexophilins, and dystrophoglycan. They exert profound effects on neurological function by mediating signalling across synapses and determining synaptic characteristics through the recruitment of additional proteins for synapse formation. Alterations in neurexin-encoding genes cause cognitive disorders such as autism, developmental delay and schizophrenia. The three neurexin genes in the human genome (NRXN1, NRXN2, and NRXN3) each have two different functional promoters, producing a large (alpha) and small (beta) transcript with corresponding proteins. NRXN1 produces hundreds, perhaps thousands, of different transcripts with differential localization in the CNS. Results We report here the identification of an individual (53825) with mild dysmorphia, severe language disorder, mild intellectual disability, attention deficit hyperactivity disorder (ADHD), and a mood disorder. Genomic analysis by Affymetrix 6.0 Gene Chip and FISH (fluorescence in situ hybridization) using probes specific for NRXN1 revealed a hemizygous deletion of approximately 190 Kb, which includes exons 3-5 of NRXN1. This deletion should result in the absence of the vast majority of different NRXN1 alpha transcripts from one of the NRXN1 gene copies, without effecting NRXN1 beta transcription.
2011-06-25 | GSE23358 | GEO