Differential expression of microRNAs in human postmortem brain tissues of MDMA addiction
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA412321 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In this study, we performed miRNA profiling of nucleus accumbens (NAc) and ventral tegmental area (VTA) in MDMA users and control postmortem human brains, which were obtained from Council of Forensic Medicine (Istanbul). According to the microarray analysis of significantly differentially expressed miR-1202 and miR-7975 were selected for further validation using quantitative reverse-transcription PCR (qRT-PCR). qRT-PCR analysis demonstrated that the expression level of miR-7975 was significantly lower in 30 VTA region of MDMA samples compared to 30 control samples. Another significantly deregulated miR-1202 was down-regulated in 30 NAc region of MDMA samples in comparison to 30 control samples. To the best of our knowledge, this is the first study demonstrating that changes in miRNA expression levels are associated with postmortem MDMA users’ brains. Alteration of these miRNAs can serve as novel biomarkers for prediction of MDMA addiction. Our findings suggest that certain differentially expressed miRNAs in MDMA seeking behavior can be used as diagnostics and therapeutic markers.
2020-03-24 | GSE104315 | GEO
Project description:Analysis of methylomic alternations related with alcohol use disorders (AUD). The hypothesis is that chronic alcohol consumption might alter genome-wide DNA methylation patterns. The results suggest that differential DNA methylation might be invovled in neuradaptations to alcohol. Genomic DNA was extraced from postmortem prefrontal cortex tissues of 23 AUD cases and 23 matched controls. Both AUD cases and matched controls are assessed with DSM-IV
2013-11-06 | E-GEOD-49393 | biostudies-arrayexpress
Project description:Analysis of transcriptiomic alternations related with alcohol use disorders (AUDs). The hypothesis is that chronic alcohol consumption might alter genome-wide gene expression patterns. The results suggest that differential gene expression in the prefrontal cortex is implicated in neuroadaptations to alcohol. Total RNAs were extracted from postmortem prefrontal cortex tissues from 23 AUD cases and 23 matched controls. Both AUD cases and matched controls were assessed with DSM-IV.
2013-11-06 | E-GEOD-49376 | biostudies-arrayexpress
Project description:Analyzing brain region differences for postmortem Alzheimer's disease tissues.
2024-06-30 | E-MTAB-14167 | biostudies-arrayexpress
Project description:To determine differential expression of microRNAs in placentae with severe pre-eclampsia and normal placenta. Differential expression of microRNAs in placentae (4 severe pre-eclampsia and 4 normal control) was screened by microarray platform, then some differential microRNAs were selected and validated with real-time quantitative reverse transcription polymerase chain reaction in placentae of severe pre-eclampsia (n=24) and normal control group (n=26). Results: We validated the expression of some microRNAs altered in the microarray, and found the following microRNAs were significantly increased in severe pre-eclampsia placentae: miR-16, miR-29b, miR-195, miR-26b, miR-181a, miR-335 and miR-222. Conclusion: These differential microRNAs may play an important role in pathogenesis of pre-eclampsia.
2011-04-14 | GSE15789 | GEO
Project description:Purpose: To investigate the role and mechanism of microRNAs in tuberculosis. Methods: microRNAs sequencing were performed to screen differential expressed microRNAs in PBMC specimen between tuberculosis patients and normal volunteers. Results: A total of 1560 distinct microRNAs were identified in these samples, and 788 of these microRNAs were upregulated and 772 microRNAs were downregulated. Overall design: Tuberculosis differential expression Profiles of microRNAs in PBMC were generated by high throughput sequencing, using Illumina Hiseq2000/2500.
2022-07-03 | GSE207244 | GEO
Project description:<p>This project characterizes DNA methylation and gene expression changes that occur in the human brain, specifically in neurons from the rostral striatum. Major advances from NIDA funded initiatives for noninvasive neuroimaging studies have made it possible to study neuroanatomical, neurochemical and functional changes in the human brain that contribute to the vulnerability to abuse drugs, together with the neurotoxic consequences of years of drug misuse. Animal models have been developed to explain the fundamental behavioral and biological mechanisms of addiction, including reward, tolerance and dependence. From these studies, we learned that cocaine abuse not only alters the epigenetic status of genes, but also induces particular epigenetic modifications depending on the frequency of the drug's administration. Certain genes are switched on by infrequent (short-term exposure) administration, while others are switched on only after chronic administration (addiction/dependence). Animal studies have also suggested that cocaine-seeking habits modeling chronic cocaine addiction in humans depend upon dopamine-dependent serial connectivity linking the ventral (nucleus accumbens) with the dorsal striatum (caudate nucleus). The primary goal of this study is to identify DNA methylation and gene expression changes that occur in the transition from recreational cocaine use to cocaine addiction. High throughput sequencing studies were designed to investigate unique postmortem human brain specimens from individuals that met criteria for cocaine dependence, as compared to unaffected age-matched controls.</p> <p>Brain biospecimens were available from the University of Miami Brain Endowment BankTM, from a collection of phenotypically well-characterized postmortem tissues sampled from chronic cocaine abusers that came to autopsy. This biobank of postmortem brain specimens and annotated genomic data serve as a research resource to support NIDA's scientific mission.</p>
| phs001377 | dbGaP
Project description:The existence of repressive and durable chromatin assemblies along gene promoters or networks, especially in the brain, is of theoretical and therapeutic relevance in a subset of individuals diagnosed with schizophrenia who experience a chronic, persistent, and treatment-resistant trajectory. We used chromatin immunoprecipitation followed by deep sequencing (ChIP-Seq) to generate an epigenomic map that includes differential sites occupied by di-methylated lysine 9 of histone 3 (H3K9me2), a repressive modification that is yet unexplored in human postmortem brain tissue. We have discovered over 150 significantly differential promoter sites in the postmortem prefrontal cortex tissue of individuals diagnosed with schizophrenia (n=15) when compared to controls (n=15). Potentially dysregulated gene categories include postsynaptic proteins, processing enzymes (for proproteins, lipids, and oxidative stress), cadherin family genes, the complement system, and peptide hormones. Ten genes with significantly increased or decreased H3K9me2 promoter occupation were selected through statistical analysis, function, or previous GWAS association, and qRT-PCR was performed on an extended sample of postmortem brain tissue, adding an additional 17 controls, 7 individuals with schizophrenia, and 19 individuals with bipolar samples (n=32 control, 22 schizophrenia, 19 bipolar). This approach revealed that mRNA expression levels correlated with chromatin modification levels in eight of ten selected genes, and mRNA expression in the total sample could be predicted by the occupancy of H3K9me2. Utilization of this method and replication in a larger sample open a pathway to durable and restrictive epigenomic assemblies whose accumulation across the lifespan of individuals diagnosed with schizophrenia may explain treatment resistance, and advance therapeutic options.
2022-10-25 | GSE215991 | GEO
Project description:Attempts to establish a tissue bank from autopsy samples have led to uncovering of the secrets of many diseases. Here, we examined the length of time that the RNA from postmortem tissues is available for microarray analysis and reported the gene expression profile for up- and down-regulated genes during the postmortem interval (PMI). We extracted RNA from fresh-frozen (FF) and formalin-fixed paraffin-embedded (FFPE) brains and livers of three different groups of mice: 1) mice immediately after death, 2) mice that were stored at room temperature for 3 h after death, and 3) mice that were stored at 4°C for 18 h after death, as this storage resembles the human autopsy process in Japan. Based on the microarray analysis, we selected genes that were altered by >1.3-fold or <0.77-fold and classified these genes using hierarchical cluster analysis following DAVID (database for annotation, visualization, and integrated discovery) gene ontology analysis. These studies revealed that cytoskeleton-related genes were enriched in the set of up-regulated genes, while serine protease inhibitors were enriched in the set of down-regulated genes. Interestingly, although the RNA quality was maintained, up-regulated genes were not validated by quantitative PCR, suggesting that these genes may become fragmented or modified by an unknown mechanism. We extracted RNA from fresh-frozen (FF) brains and livers from mice under three different conditions: 1) mice just after death as a control, 2) mice that were stored at room temperature for 3 h after death, and 3) mice that were stored at 4°C for 18 h after death to resemble the human autopsy process. We also created formalin-fixed paraffin-embedded (FFPE) tissue blocks at the same time using mouse organs obtained under the three conditions described above. We then purified RNA from the FFPE tissue blocks. Furthermore, we performed microarray analysis to examine changes in the gene expression profiles during the postmortem interval in FF samples and to compare ene expression profiles between FF and FFPE samples at three different postmortem times as described for the FF samples.
2016-05-13 | E-GEOD-78203 | biostudies-arrayexpress
Project description:Postmortem human microbiome Raw sequence reads
| PRJNA925138 | ENA