Tissue culture model of hypothermia
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE54229 | GEO | 2014/03/01
SECONDARY ACCESSION(S): PRJNA235997
REPOSITORIES: GEO
Similar Datasets
Project description:Therapeutic hypothermia is a clinically effective treatment for various hypoxic and ischemic conditions, but the associated molecular mechanisms remain unclear. To gain insight into hypothermia-induced transcriptional response, mouse embryonic fibroblasts were exposed to mild hypothermia (32°C) or normothermia (37°C) for increasing time periods. We aimed to identify genes with temporally near-monotonic response as the most obvious candidates for mediating the therapeutic effects of hypothermia. Hypothermia was compared against normothermia at seven different time-points. Hypothermic and normothermic mouse embryonic fibroblasts (MEF, in 100 mm dishes, one array per time-point) were submitted to gene expression analysis using Mouse Gene 1.0 ST GeneChip® (Affymetrix) microarrays. Differential gene expression analysis was performed with R package DEMI (http://biit.cs.ut.ee/demi/).
2014-03-01 | E-GEOD-54229 | biostudies-arrayexpress
Project description:Hypothermia affects the body in positive and negative consequences. In cardiac, hypothermia depresses myocardial contraction, slows conduction, and decreases metabolic rate. However, little is known about the molecular mechanism. Here we compare the genes expression of human adult ventricular cardiomyocyte cells (AC16) treated with hypothermia, trying to find changes under different temperatures and then elucidate the candidate genes that may play important roles in the response to hypothermia. A total of 2413 differentially expressed genes (DEGs) were identified by microarray hybridization, which provided abundant data for further analysis. Gene Ontology enrichment analysis revealed that genes related to gene transcriptions, protein and lipid metabolic were significantly enriched. KEGG analysis showed that DEGs were significantly enriched in TGF-β pathway and cytokine-cytokine receptor interaction, which may play important roles in response to hypothermia. A set of TFs (CPBP, Churchill, NF-AT1, GKLF, SRY, ZNF333, ING4, myogenin, DRI1 and CRX) was recognized to be the functional layer of key nodes, which mapped the signal of hypothermia to transcriptome. These identified DEGs, pathways and predicted TF could facilitate further investigations of the detailed molecular mechanisms, making it possible to take advantage of the potential applications of hypothermia in broader ranger AC16 cell lines was treated by hypothermia (n=3) and control group (n=3) for 6 hours.
2015-07-28 | E-GEOD-71361 | biostudies-arrayexpress
Project description:Hypothermia affects the body in positive and negative consequences. In cardiac, hypothermia depresses myocardial contraction, slows conduction, and decreases metabolic rate. However, little is known about the molecular mechanism. Here we compare the genes expression of human adult ventricular cardiomyocyte cells (AC16) treated with hypothermia, trying to find changes under different temperatures and then elucidate the candidate genes that may play important roles in the response to hypothermia. A total of 2413 differentially expressed genes (DEGs) were identified by microarray hybridization, which provided abundant data for further analysis. Gene Ontology enrichment analysis revealed that genes related to gene transcriptions, protein and lipid metabolic were significantly enriched. KEGG analysis showed that DEGs were significantly enriched in TGF-β pathway and cytokine-cytokine receptor interaction, which may play important roles in response to hypothermia. A set of TFs (CPBP, Churchill, NF-AT1, GKLF, SRY, ZNF333, ING4, myogenin, DRI1 and CRX) was recognized to be the functional layer of key nodes, which mapped the signal of hypothermia to transcriptome. These identified DEGs, pathways and predicted TF could facilitate further investigations of the detailed molecular mechanisms, making it possible to take advantage of the potential applications of hypothermia in broader ranger
2015-07-28 | GSE71361 | GEO
Project description:Background: Moderate hypothermia (32oC for 12 – 72 hours) has therapeutic applications, but the mechanisms by which it affects cellular function are unclear. We tested the hypothesis that moderate hypothermia produces broad changes in gene expression by human cells at the level of mRNA. Methods: Acute monocytic leukemia THP-1 cells were incubated under control conditions (37oC) or moderate hypothermia (32oC) for 24 hours. Cellular mRNA was extracted and a cold stress response was confirmed by examining the expression of the cold-inducible gene CIRBP by reverse transcription PCR (RT-PCR). Gene expression analysis was performed on seven sets of samples with Affymetrix U133A chips, using established statistical methods. Sequences were considered to be affected by cold if they showed statistically significant changes in expression and also met published post-hoc filter criteria (changes in geometric mean expression of 2-fold or greater and detection calls of “present” or “marginal” in at least half of the experiments). The changes in expression of a select number of these sequences were further confirmed by PCR. Results: 167 sequences met our prospectively defined criteria for a change in expression; 67 showed increases in expression and 100 showed decreases in expression. Consistent with prior literature, the cold-inducible genes CIRBP and RBM3 showed increases in expression. Functional categories affected by cold stress included genes involved in immune responses, cell growth, proliferation, and differentiation, and metabolism and biosynthesis. Several heat shock proteins (HSPs) showed decreases in expression. Conclusions: Moderate hypothermia produces substantial changes in cellular gene expression, in categories potentially of importance to systemic function. Interestingly, cold exposure without re-warming decreased the expression of several HSPs. Our in vitro findings suggest that moderate hypothermia in vivo might produce physiologically important changes in gene expression by circulating leukocytes. Keywords: Stress response / hypothermia
2006-04-05 | GSE4425 | GEO
Project description:Diagnosis of fatal hypothermia is considered to be difficult in forensic practice. In this study, in order to identify novel molecular markers of fatal hypothermia, we made rat models of mild, moderate and severe hypothermia, and performed body temperature-dependent gene expression analysis in illiopsoas muscle using next-generation sequencing.
2019-01-11 | GSE109148 | GEO
Project description:The only validated treatment to prevent brain damage associated with hypoxia-ischemia (HI) encephalopathy of the newborn is controlled hypothermia with limited benefits. Additional putative neuroprotective drug candidates include sildenafil citrate, a phosphodiesterase-type 5 inhibitor. The main objective of this preclinical study is to assess its ability to reduce HI-induced neuroinflammation, in particular through its potential effect on microglial activation. HI was induced in P10 Sprague–Dawley rats by unilateral carotid permanent artery occlusion and hypoxia (HI), and treated by either hypothermia (HT) alone, Sildenafil (Sild) alone or combined treatment (SildHT). Lesion size, glial activation were analyzed by immunohistochemistry, qRT-PCR and proteomic analyses performed at P13. Exposure to any treatment was not associated with significant reduction in lesions size both in cerebral cortex and hippocampus, 72h after HI. Significant reductions in either Iba1+ (within the ipsilateral hemisphere) or GFAP+ cells (within the ipsilateral hippocampus) were observed in SildHT group, but not in the other treatment groups. In microglia sorted cells, pro-inflammatory markers, ie. Il1b, Il6, Nos2, and CD86 were significantly downregulated in SildHT treatment group only. These changes were restricted to ipsilateral hemisphere, were not evidenced in sorted astrocytes, and were not sex-dependent. Proteomic analyses in sorted microglia refined the pro-inflammatory effect of HI and confirmed a biologically relevant impact of SildHT on specific molecular pathways including notably genes related to neutrophilic functions. Our findings demonstrate that Sildenafil combined with controlled hypothermia confers maximum effect to mitigate microglial activation induced by HI through complex proteomic regulation. The reduction of neuroinflammation induced by Sildenafil may represent an interesting therapeutic strategy for neonatal neuroprotection.
2024-04-30 | PXD045168 | Pride
Project description:Hypoxic-ischemic (HI) injury in the developing brain is a common cause of disability in children, and there are no effective treatments at this time. Exposure to sublethal hypoxic conditions (hypoxic preconditioning) 24 hours prior to hypoxic-ischemic insult is protective in the developing rat model. We have observed protective effects on brain histopathology and on long-term sensory-motor behavioral tasks. Changes in gene expression are thought to underlie this protective effect. By comparing gene expression in rats subjected to hypoxic preconditioning or sham conditioning at several time points from 0 to 24 hrs after preconditioning, we should gain insight into the mechanisms underlying these neuroprotective effects and may identify targets for therapeutic intervention. The aim of this study is to determine the effect of hypoxic preconditioning on global gene expression, and, in littermates, to examine the effect of hypoxic preconditioning 24 h prior to hypoxic-ischemic insult on brain histopathology. We hypothesize that changes in gene expression underlie the protective effect of hypoxic preconditioning against subsequent hypoxic-ischemic insult. Gene expression will be examined in two groups, 1) preconditioned and 2) sham controls, at 4 time points. On postnatal day 6, preconditioned animals are exposed to normothermic hypoxia for 3 hrs (8.0% oxygen, 36 degrees C), and sham animals are simultaneouosly exposed to normoxia at 36 degrees C. Animals are then returned to their dams until euthanized at 4 time points (0h, 2h, 8h, and 24h later). Five brains/group/timepoint will be used, with an equal number of males and females in each group. Brains are removed and dissected on ice. Cerebral cortex is dissected from both hemispheres and rapidly frozen on dry ice. Total RNA is isolated using the QIAGEN RNeasy Protect Maxi Kit. Littermates of these animals will be exposed to hypoxic preconditioning or sham preconditioning and subjected to hypoxic-ischemic injury 24 h later. These animals are euthanized at postnatal day 14 for histopathologic evaluation of injury.
2008-06-13 | E-GEOD-4753 | biostudies-arrayexpress
Project description:Transcriptomic changes in the pre-chiasmatic optic nerve, retrobulbar optic nerve of goats 1 day after hypothermia treatment of optic nerve crush injury
2022-02-24 | GSE197123 | GEO
Project description:Next-generation sequencing (NGS) has revolutionized systems-based analysis of gene expression. The goals of this study are to compare the different transcripts between control or RBM3 knockdown in the neural stem cells when the maternal hypothermia was induced.
2017-09-27 | GSE104300 | GEO
Project description:How animals rewire cellular programs to survive cold is a fascinating problem with potential biomedical implications, ranging from emergency medicine to space travel. Studying a hibernation-like response in the free-living nematode Caenorhabditis elegans, we uncovered a regulatory axis that enhances the natural resistance of nematodes to severe cold. This axis involves conserved transcription factors, DAF-16/FoxO and PQM-1, which jointly promote cold survival by upregulating FTN-1, a protein related to mammalian ferritin heavy chain (FTH1). Moreover, we show that inducing expression of FTH1 also promotes cold survival of mammalian neurons, a cell type particularly sensitive to deterioration in hypothermia. Our findings in both animals and cells suggest that FTN-1/FTH1 facilitates cold survival by detoxifying ROS-generating iron species. We finally show that mimicking the effects of FTN-1/FTH1 with drugs protects neurons from cold-induced degeneration, opening a potential avenue to improved treatments of hypothermia.
2022-10-14 | PXD034794 | Pride