Effects of Minocycline and EE in CUMS as a MDD model: transcriptomic profiles and synaptic plasticity of microglia
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA694684 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13523622_1.fastq.gz | Fastqsanger.gz | |||
| SRR13523622_2.fastq.gz | Fastqsanger.gz | |||
| SRR13523623_1.fastq.gz | Fastqsanger.gz | |||
| SRR13523623_2.fastq.gz | Fastqsanger.gz | |||
| SRR13523624_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 54 |
Similar Datasets
Project description:Two independent differential expression analyses were performed in mice subjected to chronic unpredictable mild stress (CUMS): one consisted of microglia (Cd11b+ cells) from the prefrontal cortex (PFC) and the other from the hippocampus (HC). After the CUMS protocol, minocycline, a wide spectrum antibiotic with anti-inflammatory properties, was delivered (CUMS_M group) in the drinking water/saccharine solution during 21 days. Transcriptomic profiling for a vehicle group (VEH), who spent 3 weeks in the cage with the same drinking solutions (Water/ saccharine 0.1%) and for a environmental enrichment (EE) group, that also spent 3 more weeks in the cage where enrichment materials were provided, were performed as well.
2022-06-01 | GSE165493 | GEO
Project description:Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) is a severe, drug-induced reaction that involves both the skin and viscera. To understand the immunological components of DRESS, we prospectively assessed 40 DRESS patients. The patients were evaluated for phenotype, cytokine secretion, repertoire of CD4+ and CD8+ peripheral blood T lymphocytes and viral reactivation. A subgroup of patients was analyzed using microarrays. Patients with carbamazepine- or minocycline- induced DRESS were pooled separately for analysis. RNA from total PBMCs and CD4+ and CD8+-sorted blood T cells was amplified. Expression of 894 genes of immunological interest was analyzed with a PIQOR TM arrays (Miltenyi). Gene expression was individually compared between day 0 and 90 in the minocycline-induced DRESS patients. Control groups included patients taking minocycline carbamazepine, and healthy patients without medication.
2010-07-21 | E-GEOD-23015 | biostudies-arrayexpress
Project description:Background: Major Depressive Disorder (MDD) represents a major social and economic health issue and constitutes a major risk factor for MDD suicide. The molecular pathology of suicidal depression remains poorly understood, although it has been hypothesized that regulatory genomic processes are involved in the pathology of both MDD and suicidality. Methods: Genome-wide patterns of DNA methylation were assessed in depressed MDD suicide completers (n=20) and compared to non-psychiatric, sudden-death controls (n=20) using tissue from two cortical brain regions (Brodmann Area 11 (BA11) and Brodmann Area 25 (BA25)). Analyses focussed on identifying differentially methylated regions (DMRs) associated with suicidal depression, and epigenetic variation was explored in the context of polygenic risk scores for major depression and MDD suicide. Weighted gene co-methylation network analysis was used to identify modules of co-methylated loci associated with depressed MDD suicide completers and polygenic burden for MDD and MDD suicide attempt. Results: We identified a DMR upstream of the PSORS1C3 gene, subsequently validated using bisulfite-pyrosequencing and replicated in a second set of MDD suicide samples, which is characterized by significant hypomethylation in both cortical brain regions in MDD MDD suicide cases. We also identified discrete modules of co-methylated loci associated with polygenic risk burden for MDD suicide attempt, but not major depression. MDD suicide-associated co-methylation modules were enriched among gene networks implicating biological processes relevant to depression and suicidality, including nervous system development and mitochondria function. Conclusions: Our data suggest there are coordinated changes in DNA methylation associated with MDD suicide that may offer novel insights into the molecular pathology associated with depressed MDD suicide completers.
2016-11-01 | GSE88890 | GEO
Project description:Adverse cardiac remodeling contributes to the development and progression of heart failure (HF) driven, in part, by inappropriate sympathetic nervous system activation. While blockade of β-adrenergic receptors (β-AR) is a common therapeutic strategy in HF, not all patients respond necessitating elucidation of additional therapeutic approaches. Minocycline is an FDA-approved antibiotic with pleiotropic properties, independent of its antimicrobial action, and recent evidence suggests it may act by altering gene expression via changes in miRNA expression. Therefore, we hypothesized that minocycline would prevent adverse cardiac remodeling induced by the β-AR agonist isoproterenol involving relevant alterations in the miRNA-mRNA transcriptome. Male C57BL/6J mice received Iso (30 mg/kg/d, sc) or vehicle for 21 days via osmotic minipump and daily treatment with either minocycline (50 mg/kg, ip) or sterile saline. Isoproterenol infusion induced cardiac hypertrophy, with no change in cardiac function, that was prevented by minocycline. Total mRNA sequencing revealed that isoproterenol altered gene networks associated with inflammation and metabolism while activation of fibrosis was predicted by integrated miRNA-mRNA sequencing, involving miR-21, -30a, -34a, -92a, and -150, among others. Conversely, the cardiac miRNA-mRNA transcriptome predicted inhibition of fibrosis in hearts from mice treated with minocycline plus isoproterenol involving anti-fibrotic shifts in Atf3 and Itgb6 gene expression associated with upregulation of miR-194. Consistent with these gene signatures, picrosirius red staining confirmed isoproterenol-induced cardiac fibrosis and that this was prevented by minocycline. These results demonstrate the therapeutic potential of minocycline to attenuate adverse cardiac remodeling via miRNA-mRNA-dependent mechanisms, especially related to reduced cardiac fibrosis.
2024-02-15 | GSE255532 | GEO
Project description:Minocycline is a potent modulator of retinal microglia
2015-07-17 | GSE71025 | GEO
Project description:We do this study to identify and validate the differentially expressed circRNAs in MDD patients and to evaluate their potential as diagnostic biomarkers and as novel therapeutic targets for MDD, to explore the potential clinical value and possible mechanism of circRNAs in MDD.
2022-03-21 | GSE190518 | GEO
Project description:We examined the genetic profile of postmortem brain (hippocampal) samples; 15 brains from patients diagnosed with MDD were matched to brains from healthy subjects based on gender, race and age. Gene expression profiles in the dentate gyrus and CA1 subregions of the hippocampus were assessed by cDNA hybridization to 48K human HEEBO whole genome microarrays (Microarray, Inc). Two-group comparison: MDD (13 male, 8 female) vs. Control (11 male, 7 female). Dentate Gyrus (DG): 15 pairs of samples (1 array per pair); CA1: 15 pairs of samples (1 array per pair). Biological replicates. We can not provide a list of normalized values for each individual hybridization (per chip), but rather have a list of average expression values for all hybridizations used in the experiment (n=15). See supplementary files below. CODES: AAm, African American; C, Caucasian; CO, carbon monoxide; CVD, cardiovascular disease; ETOH, ethanol; F, female; Hx, history of alcohol abuse but not currently active; M, male; MDD, Major Depressive disorder, ND, no psychotropic medication detected; NOS, not otherwise specified, OD, drug overdose; PE, prior episode of major depression with psychotic features; PMI, postmortem interval (hours); SIGSW, self-inflicted gunshot wound; [1], Psychotrophic prescriptions within last month; [2], MDD in remission; [3], prescriptions for six days prior to death; *, samples present only in array sets for the dentate gyrus; **, samples present only in array sets for CA1.
2010-10-17 | E-GEOD-24095 | biostudies-arrayexpress
Project description:Major depressive disorder (MDD) is a severe psychiatric illness that affects about 16 percent of the global population. Despite massive efforts, unravelling the pathophysiology of MDD and developing effective treatments is still a huge challenge. Here, we report a novel therapeutic axis of methylglyoxal (MGO)/tropomyosin receptor kinase B (TrkB) for treating MDD. As an endogenous metabolite, MGO was demonstrated directly binding to the extracellular domain of TrkB, provoking its dimerization and autophosphorylation. This rapidly enhances the expression of brain-derived neurotrophic factor (BDNF) and forms a BDNF-positive feedback loop. Low-dose treatment of MGO effectively promotes the hippocampal neurogenesis and exhibits sustained antidepressant effects in chronic unpredictable mild stress rat models. In addition, the modulation on MGO concentration by overexpression or inhibition of Glyoxalase 1 (GLO1) has been demonstrated associated with depression behaviors in rats. Furthermore, we also identified a natural product luteolin and its derivative lutD as potent inhibitors of GLO1 and explored their precise binding modes. Our findings reveal a novel regulatory mechanism underlying MDD and depict principles for the rational design of new antidepressants targeting GLO1.
2018-09-06 | GSE119482 | GEO
Project description:Mice were infusion with either vehicle or isoproterenol for 21 days. Another group of mice received both isoproterenol infusion and daily minocycline administration for the duration of the experiment. After 21 days mice were assessed for cardiac function and hearts collected to isolate miRNA.
2024-02-15 | GSE255838 | GEO