Mus musculus
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PROVIDER: PRJNA328246 | ENA |
REPOSITORIES: ENA
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Project description:Transcription profiling of blood, dentate gyrus and anterior cingulate cortex in mice exposed Unpredicatble Chronic Mild Stress and treated with fluoxetine
| PRJNA328242 | ENA
Project description:Groups of 8 adult BALB/c male mice were either untreated or exposed for 9 weeks to unpredicatble chronic mild stress (UCMS), or exposed for 7 weeks to UCMS and treated for the last 5 weeks with fluoxetine (Flx) diluted in drinking water, or untreated for 2 weeks and received Flx for 5 weeks. Total RNAs from whole blood (WB) were profiled after hybridization with Agilent SurePrint G3 Mouse GE 8x60K Microarray v1 to identify transcriptional biomarkers of major depression.
2017-09-14 | GSE84184 | GEO
Project description:Transcription profiling of dentate gyrus and anterior cingulate cortex in mice exposed Unpredicatble Chronic Mild Stress and treated with fluoxetine
| PRJNA328247 | ENA
Project description:Major depression is a multidimensional disorder highly prevalent in modern society. Although several classes of antidepressants (ADs) are currently available to treat depression, the effectiveness of treatment is still limited, as many patients do not show full remission; thus, there is a need to find better patients’ directed therapeutic strategies. Neuroplastic changes in several brain regions, namely in the hippocampal dentate gyrus (DG), are amongst the best correlates of depression and of ADs actions. In this study the targets and molecular mediators of chronic stress and of four ADs from different pharmacological classes (fluoxetine, imipramine, tianeptine and agomelatine) were investigated in the DG. Using the unpredictable chronic mild stress (uCMS) animal model of depression, the molecular commonalities and specificities of the ADs were determined. All ADs, except agomelatine, could reverse the behavioral deficits produced by uCMS, and the neuroplastic changes in the DG; agomelatine reversed only the anhedonic profile in the sucrose consumption test. Chronic stress induced mild but relevant molecular changes that were mostly reversed by fluoxetine, imipramine and tianeptine. Fluoxetine reduced pro-inflammatory response and increased cell metabolism pathways. Its actions were mostly dependent on molecular changes occurring in neurons. Similarities were found between imipramine and tianeptine molecular actions and targets, as both activated pathways related to cellular protection. Moreover, no particular neural cell type enrichment was found with both treatments. Agomelatine presented a very dissimilar molecular pattern impacting greatly on Rho-GTPases-related pathways in oligodendrocytes and neurons. The recognition of these molecular alterations contributes to the understanding of the processes implicated in the onset and treatment of depression and may pave the way for more effective therapeutic interventions. We compared gene expresssion in the dentate gyros of rats which were either untreated, exposed to unpredictable chronic mild stress, or exposed to the same stress and treated with either fluoxetine, imipramine, tianeptine, or agomelatine
2015-07-02 | E-GEOD-56028 | biostudies-arrayexpress
Project description:Groups of 8 adult BALB/c male mice were either untreated or exposed for 9 weeks to unpredicatble chronic mild stress (UCMS), or exposed for 7 weeks to UCMS and treated for the last 5 weeks with fluoxetine (Flx) diluted in drinking water, or untreated for 2 weeks and received Flx for 5 weeks. Total RNAs from dentate gyrus (DG) and anterior cingulate cortex (ACC) were profiled after hybridization with Agilent SurePrint G3 Mouse GE 8x60K Microarray v1 to identify transcriptional biomarkers of major depression.
2017-09-14 | GSE84183 | GEO
Project description:Gene expression profiling of blood cells in patients with major depressive disorder (MDD) has been used to identify potential biomarkers and to address the pathophysiology of MDD. However, whether alteration in gene expression in blood cells are reflected in the brain of the same individual is unclear. Here, we used an animal model of depression to investigate intra-subject correlation of gene expression patterns between the whole blood (WB) and the medial prefrontal cortex (mPFC). Ovariectomized mice exposed to the chronic mild stress were used as an animal model of depression.
2015-08-21 | GSE72262 | GEO
Project description:Rationale: Chronic obstructive pulmonary disease (COPD) is a prevalent respiratory disease lacking disease modifying treatment. The role of CXCL12/CXCR4 axis has been demonstrated in acute exacerbation of COPD. The interest of study early COPD has been recently pointed out. Objectives: To study the role of the CXCL12/CXCR4 axis in both human and mouse model of early COPD. Methods: Blood and lung tissue were obtained from both COPD patients and mice exposed to cigarette smoke (CS) for 10 weeks and intranasal instillations of polyinosinic–polycytidylic acid (poly(I:C)) to mimic exacerbations for 5 weeks. Measurements and Main Results: Exposed mice presented mild airway obstruction, peri-bronchial fibrosis and right heart remodeling. The level of CXCR4 expressing cells was increased in the blood of exposed mice, as well as in the blood of patients with mild COPD. Lung CXCL12 expression was higher both in exposed mice and COPD patients. The densities of fibrocytes expressing CXCR4 were increased in the blood and in the bronchial submucosa of exposed mice. Conditional inactivation of CXCR4 at adult stage as well as pharmacological inhibition of CXCR4 with plerixafor injections improved lung function and inflammation and protected against CS and poly-(I:C)-induced airway and cardiac remodeling. CXCR4-/- and plerixafor-treated mice also had reduced levels of CXCR4-expressing circulating cells and a lower density of peri-bronchial fibrocytes. Conclusions: We demonstrated that targeting CXCR4 has beneficial effects in an animal model of early COPD, and provide a framework to translate preclinical findings to clinical settings within a drug repurposing approach.
2025-05-12 | PXD040105 | Pride
Project description:This study aims at investigating the role of IL-17 in fluoxetine resistance in depression.The WGCNA analysis was utilized to analyze differentially expressed genes between response to antidepressant (GRA) group and resistance to antidepressant (AR)group. Furthermore, the treatment resistance model of depression was established inChronic unpredictable mild stress (CUMS) mice administrated with fluoxetine (widely used clinical medication for the treatment of depression) according to sucrose preference rate. Depression-like behaviors in mice were detected in Control group, CUMS group, GRA group, AR group, SR1001 (Th17 differentiation inhibitor) group. Subsequently, HT22 cells were exposed to IL-17 secreted by Th17 differentiation. Transcriptome sequencing from the Control and IL-17 group was used to screen differential genes. And then HT22 cells were transfected with si-JAK1 or si-STAT6. Th17 differentiation, the integrity of the blood-brain barrier (BBB), JAK1-STAT6 signaling pathway related proteins were detected by western blot, immunocytochemistry, flow cytometric analysis, ELISA experiments, immunofluorescence, and PCR. The inhibition of Th17 differentiation and the reduction of peripheral IL-17 release could increase their sensitivity to fluoxetine resistance and relieve the depression-like behavior. This process may be associated with the JAK1-STAT6 pathway.
2025-04-13 | GSE263959 | GEO
Project description:Prenatal stress is one of the risk factors for the development of mental disorders in offspring, but its underlying mechanism remains elusive. To perform epigenomic profiling of prenatal stress effects on fetal brains, ATAC-seq and RNA-seq were used to explore the changes of chromatin accessibility and gene expression on embryonic brains at E15.5 of offspring from pregnant mice, which were exposed to chronic mild unpredictable stress between E5.5 to E14.5.
2023-03-01 | GSE205087 | GEO
Project description:Gene expression profiling of blood cells in patients with major depressive disorder (MDD) has been used to identify potential biomarkers and to address the pathophysiology of MDD. However, whether alteration in gene expression in blood cells are reflected in the brain of the same individual is unclear. Here, we used an animal model of depression to investigate intra-subject correlation of gene expression patterns between the whole blood (WB) and the medial prefrontal cortex (mPFC). Ovariectomized mice exposed to the chronic ultra-mild stress were used as an animal model of depression. The major findings of the current genome-wide microarray analysis are that 1) the expression levels of 467 genes that were expressed in both tissues correlated positively between the two tissues, 2) alterations in the expression of 4,215 genes in the WB of OVX-operated mice compared to the sham-operated mice were concordant with alterations in the corresponding mPFC, 3) the biological terms over-represented in the 4,215 OVX-affected genes were associated with ribosomal function, and 4) the 6 genes that are potentially relevant to depression-like behavior were observed to be differentially expressed in the WB of the model mice. The current findings suggest that alterations in the expression of a subset of genes are significantly correlated between the WB and the mPFC with in the same individual in an experimental model of depression. Female mice were subjected to chronic ultra-mild stress, a bilateral ovariectomy, or both. Sham-operated mice without stress were used as the control. Medial prefrontal cortex and whole blood were obtained from the same individual (n = 6 in each group), and analyzed using an Agilent SurePrint G3 Mouse GE 8×60K Microarray (Design ID: 028005)
2015-08-21 | E-GEOD-72262 | biostudies-arrayexpress