Effect of chronic restraint stress or repeated activation of PVN neurons responding to restraint stress on gene expression of white adipose tissues (iWAT and eWAT) during adipogenesis of mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE216370 | GEO | 2022/10/29
REPOSITORIES: GEO
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Project description:The hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei are important integrative structures that regulate co-ordinated responses to perturbations in cardiovascular homeostasis. Through descending projections from parvocellular neurons to the brainstem, the PVN acts as an autonomic 'premotor nucleus', regulating reflex changes in sympathetic nerve activity that are involved in blood pressure and blood volume regulation. Endocrine responses are mediated through axonal projections from SON and PVN magnocellular neurons (MCNs) to the capillaries of the posterior pituitary neural lobe. In response to dehydration, a massive release of the antidiuretic peptide hormone vasopressin (VP) into the circulation is accompanied by a dramatic functional remodelling of the HNS. We have used microarrays to comprehensively catalogue the genes expressed in the PVN, the SON and the neurointermediate lobe (NIL) of the pituitary gland. Further, we have identified transcripts that are regulated as a consequence of dehydration, as well as RNAs that are enriched in either the PVN or the SON. We suggest that these differentially expressed genes represent candidate regulators and effectors of HNS activity and remodelling. Keywords: DEHYDRATION, PVN
2005-12-01 | GSE3111 | GEO
Project description:Stress is a powerful modulator of neuroendocrine, behavioral and immunological functions. After 4.5 days of repeated combined acoustic and restraint stress as a murine model of chronic psychological stress severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turn-over, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice .Thus, in our murine model, repeated stress caused severe metabolic dysregulations leading to a drastic reduction of the individualâs energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer. Endocrinology Epub ahead of print, March 11, 2008; doi:10.1210/en.2008-0038; This SuperSeries is composed of the following subset Series:; GSE11123: Mouse liver gene expression after a single acute 2h exposure to combined acoustic and restraint stress vs. control; GSE11125: Mouse liver gene expression after 4.5 days of repeated combined acoustic and restraint stress vs. control Experiment Overall Design: Refer to individual Series
2008-06-18 | E-GEOD-11126 | biostudies-arrayexpress
Project description:Rationale Electroconvulsive seizure (ECS) therapy is a nonchemical treatment for depression. Since ECS up-regulates expression of c-Fos in the paraventricular nucleus of hypothalamus (PVN), the function of which is frequently influenced in depression, we hypothesized that ECS modulates functions of the PVN and contributes to its antidepressant effects. Objectives To identify gene expression changes in the mouse PVN by ECS treatment Material and methods First, we established a method to amplify nucleotides from small quantities of RNA. Mice received one shock of ECS and their brains were collected at 2 or 6 h after shock. The PVN was microdissected from dehydrated brain sections, its total RNA was extracted and microarray analysis was applied. Results At 2 h after ECS, 2.6% (589 genes) of the probes showed more than 2-fold decrease, and 0.9% (205 genes) showed more than 2-fold increase. To confirm the expression changes, genes showing differential expression with a wide range in the microarray were analyzed by qPCR. Among the genes with more than 2-fold change by ECS, down-regulated 94 genes and up-regulated 24 genes have been reported the association with anxiety, bipolar disorder or mood disorder by the Ingenuity knowledge database. The groups of down-regulated genes, which are suggested to modulate the function of the PVN or associate to psychiatric disorders, include neuropeptides (Cck), kinases (Prkcb, Prkcc, Camk2a), transcription factors (Bcl6, Tbr1), transporters (Aqp4) and others (Fmr1). Conclusion The present results indicate that ECS treatment can modulate the functions of PVN via a series of gene expression changes, and may contribute to its antidepressant effects at least in part. Mice received one shock of ECS and their brains were collected at 2 h (PVN_ECS2h_1, PVN_ECS2h_2) or 6 h after shock (PVN_ECS6h_1, PVN_ECS6h_2). The brains of sham-treated animals were collected at 2 h after treatment (PVN_sham_1, PVN_sham_2). The PVN was microdissected from dehydrated brain sections, and its total RNA was extracted. RNA samples from two or three animals were pooled to minimize the impact of biological variance. After nucleotide amplification by the ovation amplification, the gene expression profiles were obtained by the Affymetrix microarray analysis. The microarray analysis was performed twice using different sets of animals.
2012-01-24 | E-GEOD-35259 | biostudies-arrayexpress
Project description:Rationale Electroconvulsive seizure (ECS) therapy is a nonchemical treatment for depression. Since ECS up-regulates expression of c-Fos in the paraventricular nucleus of hypothalamus (PVN), the function of which is frequently influenced in depression, we hypothesized that ECS modulates functions of the PVN and contributes to its antidepressant effects. Objectives To identify gene expression changes in the mouse PVN by ECS treatment Material and methods First, we established a method to amplify nucleotides from small quantities of RNA. Mice received one shock of ECS and their brains were collected at 2 or 6 h after shock. The PVN was microdissected from dehydrated brain sections, its total RNA was extracted and microarray analysis was applied. Results At 2 h after ECS, 2.6% (589 genes) of the probes showed more than 2-fold decrease, and 0.9% (205 genes) showed more than 2-fold increase. To confirm the expression changes, genes showing differential expression with a wide range in the microarray were analyzed by qPCR. Among the genes with more than 2-fold change by ECS, down-regulated 94 genes and up-regulated 24 genes have been reported the association with anxiety, bipolar disorder or mood disorder by the Ingenuity knowledge database. The groups of down-regulated genes, which are suggested to modulate the function of the PVN or associate to psychiatric disorders, include neuropeptides (Cck), kinases (Prkcb, Prkcc, Camk2a), transcription factors (Bcl6, Tbr1), transporters (Aqp4) and others (Fmr1). Conclusion The present results indicate that ECS treatment can modulate the functions of PVN via a series of gene expression changes, and may contribute to its antidepressant effects at least in part.
2012-01-24 | GSE35259 | GEO
Project description:The hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei are important integrative structures that regulate co-ordinated responses to perturbations in cardiovascular homeostasis. Through descending projections from parvocellular neurons to the brainstem, the PVN acts as an autonomic 'premotor nucleus', regulating reflex changes in sympathetic nerve activity that are involved in blood pressure and blood volume regulation. Endocrine responses are mediated through axonal projections from SON and PVN magnocellular neurons (MCNs) to the capillaries of the posterior pituitary neural lobe. In response to dehydration, a massive release of the antidiuretic peptide hormone vasopressin (VP) into the circulation is accompanied by a dramatic functional remodelling of the HNS. We have used microarrays to comprehensively catalogue the genes expressed in the PVN, the SON and the neurointermediate lobe (NIL) of the pituitary gland. Further, we have identified transcripts that are regulated as a consequence of dehydration, as well as RNAs that are enriched in either the PVN or the SON. We suggest that these differentially expressed genes represent candidate regulators and effectors of HNS activity and remodelling. Experiment Overall Design: In total, 10 Affymetrix Genechip Rat Genome 230 2.0 were used. The experiment compared hypothalamic supraoptic nucleus from 3 day dehydrated and control male Sprague Dawley rats (10-12 weeks). For each chip, tissue from 5 animals was pooled prior to extraction of total RNA and in total 5 chips were used for each condition using independently prepared RNA samples from separate groups of animals.
2008-06-12 | E-GEOD-3111 | biostudies-arrayexpress
Project description:Stress is a powerful modulator of neuroendocrine, behavioral and immunological functions. After 4.5 days of repeated combined acoustic and restraint stress as a murine model of chronic psychological stress severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turn-over, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice .Thus, in our murine model, repeated stress caused severe metabolic dysregulations leading to a drastic reduction of the individualâs energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer. Endocrinology Epub ahead of print, March 11, 2008; doi:10.1210/en.2008-0038 Experiment Overall Design: Two biological experiments of repeated combined acoustic and restraint stress were performed, which consist each of a repeatedly stressed group and an untreated control group. Liver RNA expression profiles were analyzed in technical duplicates using pools of 8 or 9 individual RNAs of each group.
2008-06-18 | E-GEOD-11125 | biostudies-arrayexpress
Project description:Stress is a powerful modulator of neuroendocrine, behavioral and immunological functions. After 4.5 days of repeated combined acoustic and restraint stress as a murine model of chronic psychological stress severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turn-over, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice .Thus, in our murine model, repeated stress caused severe metabolic dysregulations leading to a drastic reduction of the individualâs energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer. Endocrinology Epub ahead of print, March 11, 2008; doi:10.1210/en.2008-0038 Experiment Overall Design: Two biological experiments of a single acute exposure to combined acoustic and restraint stress were performed, which consist each of an acutely stressed group and an untreated control group. Liver RNA expression profiles were analyzed using pools of 8 or 9 individual RNAs of each group.
2008-06-18 | E-GEOD-11123 | biostudies-arrayexpress
Project description:Acute stress provides many beneficial effects whereas chronic stress contributes to a variety of human health problems. The objective of this study was to use a rodent model to uncover hippocampal gene signatures associated with prolonged chronic stress which could potentially serve as biomarkers and therapeutic targets for early diagnosis and pharmacological intervention for stress induced disease. Mice were subjected to restraint stress over 7 consecutive days and gene expression changes in the hippocampus were analyzed at 3, 12 and 24 hours following the final restraint treatment. Data indicated that mice exposed to chronic restraint stress exhibit a differential gene expression profile compared to non-stressed controls. The greatest differences were observed 12 and 24 hrs following the final stress test.
2016-11-02 | E-MTAB-2402 | biostudies-arrayexpress
Project description:Background: Current stress cardiomyopathy (SCM) has a high incidence in older adults, and the theories revolve mostly around "catecholamine myocardial toxicity" and "sympathetic hyperactivation". However, the role of the central nervous system (CNS) in the pathogenesis of stress cardiomyopathy remains unknown. Methods: We investigated the role of microglia activation in the paraventricular hypothalamic nucleus (PVN) in the development of SCM. To create a SCM model, male Sprague-Dawley (SD) rats were immobilized for 6 hours every day for a week. Electrocardiogram, cardiac electrophysiology, and echocardiography were measured to verify the changes in cardiac structure and function in rats with stress cardiomyopathy. RNA sequencing was measured to explore the changes in the hypothalamus of stress cardiomyopathy. In addition, brain and heart tissues were extracted to detect microglial activation and sympathetic activity. Results: (1) Immobilization stress successfully induced SCM in SD rats. (2) Microglia were significantly activated in the hypothalamus, as evidenced by cytosol thickened and an increased in the number of branches and specifically enriched at PVN. (3) In SCM, microglia in the PVN increased central and peripheral cardiac sympathetic activity by increasing the expression of neuroinflammatory factors. (4) It is possible that inhibiting microglia activation could suppress central and heart sympathetic activity and increase the cardiac electrical stability in SCM rats. Conclusions: Immobilization stress induced SCM in SD rats can activate hypothalamic microglia, and the activated microglia are specifically enriched at PVN, which can increase the central and peripheral sympathetic nerve activity by regulating the expression of neuro-inflammatory factor, mediate left heart dysfunction and increase the susceptibility to ventricular fibrillation.
2024-04-01 | GSE261833 | GEO
Project description:The metabolic dysfunction or irreversible metabolic changes from stress may cause body vulnerability, potentially leading to the onset of psychiatric and non-psychiatric illnesses. Nevertheless, little is known about the biochemical events that cause depression due to stress. Our study employed open field test, plasma adrenocorticotropic hormone (ACTH) and corticosterone determination, serum biochemical analysis, quantitative PCR, immunoblotting, enzyme activity assay, and NMR-based metabolomics to analyze and identify the biochemical variations of body fluids (serum and urine) and tissues (brain, kidney, liver, lung, and spleen) in an acute restraint stress-induced rat model of depression. Our data suggested that the post-stress effects on biochemical alterations involved different biochemical pathways, including regulating the NAD(P) pool, glucose homeostasis, biosynthesis and degradation of heme, and uric acid production and metabolism. The urinary excretion of nicotinate and nicotinamide N-oxide increased significantly. Thus, we conclude that the depletion of NAD(P) precursors may occur in response to restraint stress. Our results show a close association between NAD(P) deficiency and post-stress metabolic dysfunction, which would provide a ground for developing recovery-promoting micronutrients in treating depression.
2022-07-30 | ST002298 | MetabolomicsWorkbench