Effect of restraint stress on gene expression in peripheral blood cells of mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE210252 | GEO | 2022/08/06
REPOSITORIES: GEO
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Project description:In response to elevated glucocorticoid levels, erythroid progenitors rapidly expand to produce large numbers of young erythrocytes. Previous work demonstrates hematopoietic changes in rodents exposed to various physical and psychological stressors, however, the effects of chronic psychological stress on erythropoiesis has not be delineated. We employed laboratory, clinical and genomic analyses of a murine model of chronic restraint stress (RST) to examine the influence of psychological stress on erythropoiesis. Mice exposed to RST demonstrated markers of early erythroid expansion involving the glucocorticoid receptor. In addition, these RST-exposed mice had increased numbers of circulating reticulocytes and increased erythropoiesis in primary and secondary erythroid tissues. Mice also showed increases in erythroid progenitor populations and elevated expression of the erythroid transcription factor KLF1 in these cells. Together this work describes some of the first evidence of psychological stress affecting erythroid homeostasis through glucocorticoid stimulation and begins to define the transcription factor pathway involved.
2016-06-07 | GSE47725 | GEO
Project description:Genome-wide transcriptional profiling results were used to examine the effect of a psychological stress paradigm for rodents (chronic restraint) on indicies of biological aging in murine femoral bone marrow leukocytes and to assess the extent to which propranolol could block such effects.
2021-03-31 | GSE157133 | 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: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: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: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 individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer. Keywords: stress response
2008-06-01 | GSE11125 | GEO
Project description:As an attempt to assess physio-psychological effects elicited in odorant-inhaled rats, gene expression profiling in the central nervous system was carried out with rats housed under stressful conditions. (R)-(-)-linalool inhalation to rats during 2 h restraint significantly up-regulated the expression of genes in hypothalamus, which were found to be related to neuron differentiation and regulation of transcription as well as immediate early genes. The expressions of 104 among focused stress-regulated genes were significantly altered by the inhalation. The (R)-(-)-linalool inhalation significantly repressed the restraint-induced changes in the expression levels of 77 of the 104. It also promoted the expression of the remaining 27 genes including those related to anti-apoptotic heat shock proteins. The differences in their hypothalamic gene expressions revealed that the inhaled odorants actually influenced stress responses, based on the restraint-induced hypothalamic gene expressions related to apoptosis. These results indicate that the analysis of gene expression profiles in rats subjected to a stressful condition is useful to evaluate odorant-induced effects as shown by the particular results that (R)-(-)-linalool inhalation under only 2 h restraint- stressed condition induces neuron differentiation against apoptosis.
2010-06-26 | GSE19589 | 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 individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer. This SuperSeries is composed of the SubSeries listed below.
2008-06-01 | GSE11126 | 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 individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer. Keywords: stress response
2008-06-01 | GSE11123 | GEO