Targeting c-Jun orchestrates heat stroke induced myocardial injury and reveals its biomarker potential
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE303366 | GEO | 2025/07/26
REPOSITORIES: GEO
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Project description:These experiments were designed to detect transcript (mRNA) changes in whole circulating blood in animals exposed to D-amphetamine under neurotoxic and non-neurotoxic conditions, or subjected to elevated environmental temperatures that produced a hyperthermia very similar to heat stroke. The study objectives were: 1) to detect transcript changes in blood due to life-threatening hyperthermia produced by elevated environmental temperatures (39°C, produces no or minimal neurotoxicity); 2) detect transcripts that could serve as biomarkers specific for neurotoxic amphetamine exposures and not seen with environmentally-induced hyperthermia; and 3) determine the transcript changes related to the immune system in circulating blood produced by either non-neurotoxic or neurotoxic amphetamine exposures. Amphetamine effects on gene expression are dependent on body temperature and indicate that many significant changes in genes related to the immune system occur, some likely in response to damage, even when animals remain normothermic during amphetamine exposure. Also, hyperthermia alone produces many changes in immune related genes in blood
2015-12-08 | GSE64778 | GEO
Project description:These experiments were designed to produce the appropriate controls so that their cohort's transcript (mRNA) changes in whole circulating blood could be determined. The cohorts were exposed to D-amphetamine under a neurotoxic and non-neurotoxic condition or subjected to elevated environmental temperatures that produced a hyperthermia very similar to heat stroke. The cohort data is in a separate, but linked, GEO file.
2015-12-08 | GSE62368 | GEO
Project description:These experiments were designed to detect transcript (mRNA) changes in whole circulating blood in animals exposed to D-amphetamine under neurotoxic and non-neurotoxic conditions, or subjected to elevated environmental temperatures that produced a hyperthermia very similar to heat stroke. The study objectives were: 1) to detect transcript changes in blood due to life-threatening hyperthermia produced by elevated environmental temperatures (39°C, produces no or minimal neurotoxicity); 2) detect transcripts that could serve as biomarkers specific for neurotoxic amphetamine exposures and not seen with environmentally-induced hyperthermia; and 3) determine the transcript changes related to the immune system in circulating blood produced by either non-neurotoxic or neurotoxic amphetamine exposures. Amphetamine effects on gene expression are dependent on body temperature and indicate that many significant changes in genes related to the immune system occur, some likely in response to damage, even when animals remain normothermic during amphetamine exposure. Also, hyperthermia alone produces many changes in immune related genes in blood Five groups of animals were necessary to meet the study objectives. All groups were given 4 injections of either normal saline or amphetamine, and the injections were sequentially given with 2 h between each injection. Dosing started at 7:30 to 8:30 a.m. The groups are: 1) normothermic controls given normal saline in a 22.5°C environment; 2) controls given normal saline in a 16°C environment (also remained normothermic); 3) environmentally-induced hyperthermia given saline in a 39°C environment; 4) non-neurotoxic amphetamine given in a 16°C environment and 5) neurotoxic amphetamine group given amphetamine in a 22.5°C environment. Note the the saline controls (normothermic data) is contained in a separate but linked GEO file GSE62368
2015-12-08 | E-GEOD-64778 | biostudies-arrayexpress
Project description:Targeting c-Jun orchestrates heat stroke induced myocardial injury and reveals its biomarker potential
| PRJNA1294902 | ENA
Project description:Heat stroke is a life-threatening condition characterized by loss of thermoregulation and severe elevation of core body temperature, which can cause organ failure and damage to the central nervous system. While no definitive test exists to measure heat stroke severity, immune challenge is known to increase heat stroke risk, although the mechanism of this increased risk is unclear. In this study, we used a mouse model of classic heat stroke to test the effect of immune challenge on pathology. Employing multivariate supervised machine learning to identify patterns of molecular and cellular markers associated with heat stroke, we found that prior viral infection simulated with poly I:C injection resulted in heat stroke presenting with high levels of factors indicating coagulopathy. Despite a decreased number of platelets in the blood, platelets are large and non-uniform in size, suggesting younger, more active platelets. Levels of D-dimer and soluble thrombomodulin were increased in more severe heat stroke, and in cases presenting with the highest level of organ damage markers D-dimer levels dropped, indicating potential fibrinolysis-resistant thrombosis. Genes corresponding to immune response, coagulation, hypoxia, and vessel repair were up-regulated in kidneys of heat-challenged animals, and these increases correlated with both viral treatment and distal organ damage while appearing before discernible tissue damage to the kidney itself. We conclude that heat stroke-induced coagulopathy may be a driving mechanistic force in heat stroke pathology, especially when exacerbated by prior infection, and that coagulation markers may serve as an accessible biomarker for heat stroke severity and therapeutic strategies.
2020-05-15 | GSE129188 | GEO
Project description:These experiments were designed to produce the appropriate controls so that their cohort's transcript (mRNA) changes in whole circulating blood could be determined. The cohorts were exposed to D-amphetamine under a neurotoxic and non-neurotoxic condition or subjected to elevated environmental temperatures that produced a hyperthermia very similar to heat stroke. The cohort data is in a separate, but linked, GEO file. Animals were given four doses of 1 ml/ kg of normal saline with two hours in between each dose. The animals body temperature was determined every 1 h and the rats were sacrificed 3 h after the last saline injection. Animals were not given access to food or water during this period so that they were more suitable controls for the amphetamine treatment groups
2015-12-08 | E-GEOD-62368 | biostudies-arrayexpress
Project description:We have used microarrays to investigate the changes in gene expression at various times after stroke. Our findings reported that gene expression screening can detect known and unknown transcriptional features of stroke. Brain samples were obtained from 9 patients who died from stroke, with the approval of the local Ethics Committee. The patients were aged between 51 and 86 years and had survived between 2-37 days following stroke. Tissue samples were taken from infarct and peri-infarcted zones while controls were obtained from the contralateral hemisphere. We established mRNA expression profiles of the damaged brain tissues between 2 to 6 days, 9 to 20 days, and 26 to 37 days after stroke. RNA from three stroke patients was pooled for each patient survival group.
2010-06-25 | E-GEOD-9391 | biostudies-arrayexpress
Project description:Neuroinflammation is a hallmark of ischemic stroke, which is a leading cause of death and longterm disability. Understanding the exact cellular signaling pathways that initiate and propagate neuroinflammation after stroke will be critical for developing immunomodulatory stroke therapies. In particular, the precise mechanisms of inflammatory signaling in the clinically relevant hyperacute period, hours after stroke, have not been elucidated. We used the RiboTag technique to obtain Astrocyte IP and microglia-derived mRNA transcripts in a hyperacute (4 hours) and acute (3 days) period after stroke, as these two cell types are key modulators of acute neuroinflammation. Microglia initiated a rapid response to stroke at 4 hours by adopting an inflammatory profile associated with the recruitment of immune cells. The hyperacute Astrocyte IP profile was marked by stress response genes and transcription factors, such as Fos and Jun, involved in pro-inflammatory pathways such as TNF-α. By 3 days, microglia shift to a proliferative state and Astrocyte IPs strengthen their inflammatory response. The Astrocyte IP pro-inflammatory response at 3 days is partially driven by the upregulation of the transcription factors C/EBPβ, Spi1, and Rel, which comprise 25% of upregulated transcription factor-target interactions. Surprisingly, few sex differences across all groups were observed. Expression and log2 fold data for all sequenced genes are available on a user-friendly website for researchers to examine gene changes and generate hypotheses for stroke targets. Taken together our data comprehensively describe the Astrocyte IP and microglia-specific translatome response in the hyperacute and acute period after stroke and identify pathways critical for initiating neuroinflammation.
2023-02-14 | GSE225110 | GEO
Project description:Stroke is a “brain attack” cutting off vital blood, and consequently the nutrients and oxygen vital to the brain cells that control everything we do. Stroke is a complex disease with unclear pathogenesis resulting from environmental and genetic factors. To better understand IS´s etiology, we performed genomic expression profiling of patients and controls. Gene expression profiling was performed in peripheral blood mononuclear cells (PBMCs) of 20 IS patients and 20 sex- and age-matched controls using Affymetrix microarrays.
2011-12-31 | E-GEOD-22255 | biostudies-arrayexpress
Project description:Stroke is a “brain attack” cutting off vital blood, and consequently the nutrients and oxygen vital to the brain cells that control everything we do. Stroke is a complex disease with unclear pathogenesis resulting from environmental and genetic factors. To better understand IS´s etiology, we performed genomic expression profiling of patients and controls.
2011-12-31 | GSE22255 | GEO