Sabba-affy-rat-168529
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE4038 | GEO | 2006/01/13
SECONDARY ACCESSION(S): PRJNA95167
REPOSITORIES: GEO
Similar Datasets
Project description:Stress is a major risk factor for many cardiovascular and neuropsyhological disorders, and involved changes in gene expression; Determine target genes affected by single or repeated immboilization stress. Stress triggers alterations in gene expresssion of many proteins, especially transcription factors. The target genes of repeated stress partially overlap, but differ from those altered by single stress. Sprague Dawley male rats were exposed to single 2 hr immobilization stress or 2 hrs immbolization stress each for six consecultive days. Controls for single stress were untreated, and controls for repeated stress were handled for six days.
2008-06-12 | E-GEOD-4038 | biostudies-arrayexpress
Project description:Microarray profiling single and repeated immobilization stress responses in gene expression in rat adrenal medulla Experiment Overall Design: Immobilization stress (IMO) was performed with 2-hour once and 2-hour daily for 6 days repeated. Control groups were not exposed to stress (absolute controls). Following the last IMO, rats were euthanized by decapitation and both adrenal medulla tissues were dissected from the animal. Total RNA were isolated and the array experiments were done by Affymetrix. Data analysis will be performed by GeneTraffic program.
2008-10-18 | E-GEOD-8184 | biostudies-arrayexpress
Project description:Microarray profiling single and repeated immobilization stress responses in gene expression in rat adrenal medulla Keywords: Stress responses
2008-07-15 | GSE8184 | GEO
Project description:Stress leads to important adaptive physiological responses including release of catecholamine from the adrenal medulla. Repeated or prolonged stess increses the propensity for many disorders including cardiovascular disease and neuropsychiatric disorders. The susceptibility to stress is determined by a number of factors including prior experience with stress. It has been found that while there is adaptation to prolonged cold stres; it leads to sensitization when cold stressed animals are exposed to a different (novel) stressor. Our study aims to determine the mechanis of this adaptatio and sensitization. We will determine teh gene expression patterns in rat adrenal medulla in response to severa times of cold stress. We will also determine the changes in gene expresion with single immobilization stress in adrenal medulla of rat with an dwithout preexposure to cold stress to investigate the mechanism of sensitizatio in cold adapted animals. We hypothesize that during the course of cold stess there are alterations in gene expression of several neurotransmitter related genes and transcription factors. In expression of several trascription factors, such as Fra-2 which lead to an exaggerated response to teh novel stresor. Rats were exposed to cold stress (4 degree C) for 1, 7, or 28 days. A parallel group was kept at room temperature (unstressed). Unstressed or rats preexposed to 28 days cold were immobilized for 2 hrs and killed by decapitation. The adrenal medullae, separatedly from right and left side, have been dissected and individually frozen at - 70 degree C. We will pool samples from 4 rats per treatment to control for variability. Keywords: dose response
2006-06-09 | GSE5033 | GEO
Project description:Profiling Single and Repeated Immobilization Stress Responses in Gene Expression
| PRJNA101085 | ENA
Project description:Here we present molecular mechanisms of Korean red ginseng (KRG) on immobilization stresses Keywords: stress response Mice were divided into three groups (3 mice / group): control, stress + no treat, and stress + Korean Red Ginseng (KRG, 100 mg). Stress + KRG group were given KRG 100 mg orally for 7 days and then exposed to immobilization stress for 45 min. stress + no treat group were administrated with phosphate buffer saline (d-PBS, pH 7.4) together with IMO stress for 45 min.
2010-05-15 | E-GEOD-12656 | biostudies-arrayexpress
Project description:Stress leads to important adaptive physiological responses including release of catecholamines from the adrenal medulla. Repeated or prolonged stress increases the propensity for many disorders including cardiovascular disease and neuropsychiatric disorders. The susceptibility to stress is determined by a number of factors including prior experience with stress. It has been found that while there is adaptation to prolonged cold stress; it leads to sensitization when cold stressed animals are exposed to a different (novel) stressor. Our study aims to determine the mechanism of this adaptation and sensitization.,We will determine the gene expression patterns in rat adrenal medulla in response to several times of cold stress. We will also determine the changes in gene expression with single immobilization stress in adrenal medulla of rat with and without preexposure to cold stress to investigate the mechanism of sensitization in cold adapted animals. ,We hypothesize that during the course of cold stress there are alterations in gene expression of several neurotransmitter related genes and transcription factors. In cold adapted animals, there is increased susceptibility to stress due to sustained changes in expression of several transcription factors, such as FRA-2 which lead to an exaggerated response to the novel stressor. ,Rats were exposed to cold stress (4oC) for 1, 7 or 28 days. A parallel group was kept at room temperature (unstressed). Unstressed or rats pre-exposed to 28 days cold were immobilized for 2 hrs and killed by decapitation. The adrenal medullae, separately from right and left side, have been dissected and individually frozen at -70oC. Our recent immunoblots with the tissue from one side revealed that there is increase in tyrosine hydroxylase and c-fos with the short term cold stress and in dopamine beta hydroxylase and Fra-2 even with the prolonged cold stress. The response of several transcription factors to immobilization stress was enhanced in the cold adapted animals. RNA will be prepared with RNAqueous-Micro Isolation kit from Ambion (alternatively we can ship the tissues). We will pool samples from 4 rats per treatment to control for variability.
2007-09-28 | E-GEOD-2875 | biostudies-arrayexpress
Project description:Stress leads to important adaptive physiological responses including release of catecholamines from the adrenal medulla. Repeated or prolonged stress increases the propensity for many disorders including cardiovascular disease and neuropsychiatric disorders. The susceptibility to stress is determined by a number of factors including prior experience with stress. It has been found that while there is adaptation to prolonged cold stress; it leads to sensitization when cold stressed animals are exposed to a different (novel) stressor. Our study aims to determine the mechanism of this adaptation and sensitization. We will determine the gene expression patterns in rat adrenal medulla in response to several times of cold stress. We will also determine the changes in gene expression with single immobilization stress in adrenal medulla of rat with and without preexposure to cold stress to investigate the mechanism of sensitization in cold adapted animals. We hypothesize that during the course of cold stress there are alterations in gene expression of several neurotransmitter related genes and transcription factors. In cold adapted animals, there is increased susceptibility to stress due to sustained changes in expression of several transcription factors, such as FRA-2 which lead to an exaggerated response to the novel stressor. Rats were exposed to cold stress (4oC) for 1, 7 or 28 days. A parallel group was kept at room temperature (unstressed). Unstressed or rats pre-exposed to 28 days cold were immobilized for 2 hrs and killed by decapitation. The adrenal medullae, separately from right and left side, have been dissected and individually frozen at -70oC. Our recent immunoblots with the tissue from one side revealed that there is increase in tyrosine hydroxylase and c-fos with the short term cold stress and in dopamine beta hydroxylase and Fra-2 even with the prolonged cold stress. The response of several transcription factors to immobilization stress was enhanced in the cold adapted animals. RNA will be prepared with RNAqueous-Micro Isolation kit from Ambion (alternatively we can ship the tissues). We will pool samples from 4 rats per treatment to control for variability. Keywords: dose response
2005-07-06 | GSE2875 | GEO
Project description:Stress leads to important adaptive physiological responses including release of catecholamine from the adrenal medulla. Repeated or prolonged stess increses the propensity for many disorders including cardiovascular disease and neuropsychiatric disorders. The susceptibility to stress is determined by a number of factors including prior experience with stress. It has been found that while there is adaptation to prolonged cold stres; it leads to sensitization when cold stressed animals are exposed to a different (novel) stressor. Our study aims to determine the mechanis of this adaptatio and sensitization. We will determine teh gene expression patterns in rat adrenal medulla in response to severa times of cold stress. We will also determine the changes in gene expresion with single immobilization stress in adrenal medulla of rat with an dwithout preexposure to cold stress to investigate the mechanism of sensitizatio in cold adapted animals. We hypothesize that during the course of cold stess there are alterations in gene expression of several neurotransmitter related genes and transcription factors. In expression of several trascription factors, such as Fra-2 which lead to an exaggerated response to teh novel stresor. Rats were exposed to cold stress (4 degree C) for 1, 7, or 28 days. A parallel group was kept at room temperature (unstressed). Unstressed or rats preexposed to 28 days cold were immobilized for 2 hrs and killed by decapitation. The adrenal medullae, separatedly from right and left side, have been dissected and individually frozen at - 70 degree C. We will pool samples from 4 rats per treatment to control for variability.
2008-06-13 | E-GEOD-5033 | biostudies-arrayexpress
Project description:In skeletal muscle, the pattern of electrical activity regulates the expression of proteins involved in synaptic transmission, contraction and metabolism. Disruptions in electrical activity, resulting from prolonged bed-rest, cast-immobilization or trauma, inevitably lead to muscle atrophy. The mechanisms that regulate muscle atrophy are poorly understood, but it seems likely that changes in gene expression play a key role in initiating and maintaining a muscle atrophy program. Previously, we found that Runx1, a transcription factor previously termed AML1, was substantially induced in muscle following denervation. More recently, we sought to determine whether this increase in Runx1 expression may be causally related to the morphological changes in skeletal muscle that accompany muscle disuse, notably muscle atrophy. We found that Runx1 is indeed required to sustain muscle and to minimize atrophy following denervation. Experiments described here are designed to identify the genes that are regulated by Runx1 in skeletal muscle with the particular goal of identifying genes that regulate muscle atrophy. We propose to use microarray analysis to identify genes, expressed in skeletal muscle, that are mis-regulated in mice lacking Runx1. We inactivated runx1 selectively in skeletal muscle and found that denervated myofibers in mutant mice atrophy far more (90% atrophy) than in wild-type mice (30% atrophy). We therefore reason that Runx1 activates and/or represses genes that are required to sustain muscle and to minimize atrophy. We generated MCK::cre; runx1f/- and runx1f/- control mice. In normal mice, an increase in runx1 expression is detected by two days after denervation and is maximal by five days after denervation. Muscle atrophy is first evident between one and two weeks after denervation. As we wish to avoid detecting global changes in gene expression that are associated with late stages of muscle atrophy, we plan to denervate muscle for three or five days and to compare gene expression in dissected innervated and denervated muscles from mutant and control mice. We will generate thirty samples for comparison-5 replicates per condition: Samples 1-3 from runx1f/- control mice. (1) innervated tibialis anterior muscles (TA); (2) 3-day-denervated TA; (3) 5-day-denervated TA. Samples 4-6 from MCK::cre; runx1f/- mice. (4) innervated TA; (5) 3-day-denervated TA; (6) 5-day-denervated TA. We obtain sufficient total RNA (10 micrograms) from each dissected muscle to avoid pooling samples. We will analyze adult mice of the same age (~six weeks after birth; most will be littermates) and sex-male. It is difficult to anticipate how many genes will be identified in this screen, as few target genes for Runx1 have been identified in any cell type and none in skeletal muscle. Moreover, although we would prefer to focus our attention on genes that are strongly dependent upon Runx1 expression (e.g. more than 5-fold difference in expression in wild-type and mutant mice), we do not know the extent to which target gene expression will depend upon Runx1. For these reasons, in these experiments, we will analyze expression from five “identical” samples, so that we can be confident that even small (e.g. three-fold) differences in expression can be reliably determined. Importantly, in order to confirm results obtained from the microarray data, we will use other assays (RNase protection) to measure RNA expression of candidate genes in innervated and denervated muscles of wild-type and mutant mice. Keywords: other
2006-03-08 | GSE4411 | GEO