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Gene expression signatures in heart tissues of mice simulating posttraumatic stress disorder (PTSD) [Study2]

ABSTRACT: Using a PTSD mouse model, we investigated the longitudinal transcriptomic changes in heart tissues after the exposure to stress through intimidation We designed our time-course study (Study II) with three experimental conditions where we varied the length of time that subservient mice were exposed to aggressor mice with the same length of rest time after the exposure (1day). The conditions included were 1day-exposure (T1R1), 2day-exposure (T2R1) and 3day-exposure (T3R1).

ORGANISM(S): Mus musculus

SUBMITTER: Ji-Hoon Cho

PROVIDER: E-GEOD-52871 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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miRNA expression signatures in heart tissues of mice simulating posttraumatic stress disorder (PTSD) [Study2]

Project description:Using a PTSD mouse model, we investigated the longitudinal transcriptomic changes in heart tissues after the exposure to stress through intimidation We designed our time-course study (Study II) with three experimental conditions where we varied the length of time that subservient mice were exposed to aggressor mice with the same length of rest time after the exposure (1day). The conditions included were 1day-exposure (T1R1), 2day-exposure (T2R1) and 3day-exposure (T3R1). We designed our initial study (Study I) with four experimental conditions where we varied the length of time that subservient mice were exposed to aggressor mice and the length of rest time after the exposure. The conditions included were short exposure-short rest (T5R1-T indicates the number of days of trauma exposure; R indicates the number of days of rest after exposure), short exposure-long rest (T5R10), long exposure-short rest (T10R1) and long exposure-long rest (T10R42)

2013-12-04 | E-GEOD-52872 | biostudies-arrayexpress

Gene expression signatures in heart tissues of mice simulating posttraumatic stress disorder (PTSD) [Study1]

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miRNA expression signatures in heart tissues of mice simulating posttraumatic stress disorder (PTSD) [Study1]

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Expression signatures in heart tissues of mice simulating posttraumatic stress disorder (PTSD)

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-12-04 | E-GEOD-52875 | biostudies-arrayexpress

Liver Transcriptomics data from mouse model with Features of Post-traumatic Stress Disorder

Project description:We have used a social defeat (SD) mouse model of post-traumatic stress disorder (PTSD) that is based on a brief exposure of a mouse to the aggressor mice for either 5 d or 10 d stress periods. Mice simulating aspects of posttraumatic stress disorder exhibit behavioral changes, body weight gain, increased body temperature, and inflammatory and fibrotic histopathologies and transcriptomic changes of heart tissue. Liver tissue of these mice was subjected to mRNA analysis. Transcriptomic analysis of liver indicated chronic toxicities and metabolic alterations in aggressor-exposed mice that possibly contributed to the persistent metabolic disturbance Two-condition experiment, C57BL6/J mice Biological replicates: 4-6 control replicates, 5-6 stressed replicates.

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Exposure to ionizing radiation induced persistent gene expression changes in mouse mammary gland

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Transcription profiling of mouse liver after combined acoustic and restraint stress compared to non-stressed control mice

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

Transcription profiling of mouse liver after 4.5 days of repeated combined acoustic and restraint stress vs. control

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

Comparison of the Global Gene Expression of Choroid Plexus and Meninges and Associated Vasculature under Control Conditions and after Pronounced Hyperthermia or Amphetamine Toxicity

Project description:These tissue were harvested to complement and extend the studies that generated GSE23093. They served 3 purposes; 1) identify genes important to choroid plexus function and compare them with those important for meninges and associated vasculature (MAV) function, 2) determine genes in the choroid plexus and sensitivity hyperthermia and amphetamine toxicity, 3) identify the important gene expression changes related to the immune system in MAV, choroid plexus and trunk' blood Gene mRNA expression patterns in choroid plexus and trunk blood were determined under control conditions as well as after (3 hr and 1day) exposure to either environmentally-induced hyperthermia or neurotoxic doses of amphetamine. This data was analyzed and compared to data from meninges and associated vasculature previously deposited in GEO. The data gathered under control conditions was used to further understand how the choroid plexus and meninges and associated vasculature might function to generate and regulate the cerebrospinal fluid. The expression patterns in the choroid plexus after environmentally-induced hyperthermia or neurotoxic doses of amphetamine was determine its damage and protective responses. The expression patterns after environmentally-induced hyperthermia or neurotoxic doses of amphetamine were compared among choroid plexus, meninges and associated vasculature and blood were analyzed to determine immune system responses.

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