Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA352072 | ENA |
REPOSITORIES: ENA
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Project description:The study aimed to investigate the effect of limited fluid resuscitation on gene profiles of rat hepatic tissue. Limited fluid resuscitation can reduce mortality resulting from traumatic hemorrhagic shock. However, the protective mechanism of limited fluid resuscitation is not very clear. The rats were subjected to uncontrolled hemorrhagic shock and resuscitated with limited fluid resuscitation or aggressive fluid resuscitation. Following 5 h of resuscitation, hepatic RNA was isolated, and gene expression profiles were measured using a NimbleGen microarray. Gene ontology (GO) and pathway analyses were performed. Real-time reverse transcription polymerase chain reaction was used to verify the microarray findings. A total of 449 differentially expressed genes between aggressive fluid resuscitation and limited fluid resuscitation groups were found. The GO analysis of differential gene expression predicted a significant downregulation of response to stress, alcohol biosynthetic process, response to wounding, gluconeogenesis, hexose biosynthetic process, acute inflammatory response, inflammatory response, response to oxygen levels, glucose metabolic process, acute-phase response, and so forth, and upregulation of steroid biosynthetic process, sterol metabolic process, steroid metabolic process, alcohol metabolic process, lipid metabolic process, cholesterol metabolic process, glycogen catabolic process, glucan catabolic process, cellular polysaccharide catabolic process, monocarboxylic acid metabolic process, and so on. This study showed that limited fluid resuscitation can downregulate the expression of injury-associated differentially expressed genes and upregulate the expression of metabolism-associated differentially expressed genes, which may account for the attenuation of the deleterious effects and overall prosurvival effects of limited fluid resuscitation on uncontrolled hemorrhagic shock.
2016-11-02 | GSE89406 | GEO
Project description:A dual platform microarray analysis was used to characterize the temporal transcriptomic response in the mouse liver following trauma and hemmorhagic shock Mice were divided into five groups, anesthetized and surgically treated to simulate a time course and trauma severity model: non-manipulated animals (C), minor trauma (MT), 1.5 hour of hemorrhagic shock and severe trauma (HS/T), 1.5 hour HS/T followed by 1 hour resuscitation (HS/T+1.0R), 1.5 hour HS/T followed by 4.5 hours resuscitation (HS/T+4.5R)
2011-01-24 | E-GEOD-26695 | biostudies-arrayexpress
Project description:A dual platform microarray analysis was used to characterize the temporal transcriptomic response in the mouse liver following trauma and hemmorhagic shock Mice were divided into five groups, anesthetized and surgically treated to simulate a time course and trauma severity model: non-manipulated animals (C), minor trauma (MT), 1.5 hour of hemorrhagic shock and severe trauma (HS/T), 1.5 hour HS/T followed by 1 hour resuscitation (HS/T+1.0R), 1.5 hour HS/T followed by 4.5 hours resuscitation (HS/T+4.5R)
2011-01-24 | E-GEOD-26696 | biostudies-arrayexpress
Project description:We sequenced liver mRNA from 23 individual pigs (5 prefed and 18 fasted) taken at 4 separate time points to evaluate the change in gene expression over the course of hemorrhagic shock and resuscitation in response to a carbohydrate prefed state.
2014-03-07 | GSE55674 | GEO
Project description:We previously demonstrated in rodents that T/HS results in liver injury that can be prevented by IL-6 administration at the start of resuscitation, however the mechanism(s) for the IL-6 protective effect is not fully known. We used microarrays to detail the global gene expression in response to T/HS and the effect of IL-6 on this model with and without pharmacologic blockade of Stat3-mediated IL-6 and identified distinct members of the inflammasome de-regulated during T/HS that normalized with IL-6 administration during resuscitation. Adult male rats were subjected to either sham procedure, a trauma plus hemorrhagic shock (T/HS) procedure, T/HS with IL-6 versus PBS during resuscitation, or pretreatment with pharmacologic blockade of Stat3-mediated IL6 via GQ-ODN and after procedural completion, animals were sacrificed and livers were taken and homegenized for RNA extraction and microarray analysis using Affymetrix Rat 230A GeneChipM-BM-. array
2011-03-16 | E-GEOD-27978 | biostudies-arrayexpress
Project description:Hemorrhagic shock with injury results in alterations of the metabolic state of an organism, which contribute to organ dysfunction and death. Previous investigations have explored the effects of carbohydrate prefeed in murine models but few in clinically relevant large animal models. We performed carbohydrate prefeed in pigs undergoing simulated polytrauma and hemorrhagic shock with resuscitation to determine if carbohydrate prefeeding if the metabolic response to shock is dependent on fed state. Sixty-four Yorkshire pigs were divided into two experimental groups: fasted and prefed in additon to two Control groups. Experimental animals were subjected to a standardized hemorrhagic shock protocol, including pulmonary contusion and liver crush injury. To determine molecular alterations in response to trauma as a result of prefeeding, liver and muscle biopsies in addition to serum and urine samples were obtained at set timepoints throughout the procedure. The samples were prepared and analyzed by NMR spectroscopy.
2015-01-31 | MTBLS123 | MetaboLights
Project description:A shotgun label-free quantitative proteomic approach was utilized to compare the peptidome of plasma samples from healthy and hemorrhagic shock pigs to verify the possible role of uncontrolled proteolytic activity in shock.
2021-09-08 | PXD008018 | Pride
Project description:The etiology of trauma-hemorrhage shock-induced acute lung injury has been difficult to elucidate due, at least in part, to the inability of in vivo studies to separate the non-injurious pulmonary effects of trauma-hemorrhage from the tissue injurious ones. To circumvent this in vivo limitation, we utilized a model of trauma-hemorrhagic shock (T/HS) in which T/HS-lung injury was abrogated by dividing the mesenteric lymph duct. In this way, it was possible to separate the pulmonary injurious response from the non-injurious systemic response to T/HS by comparing the pulmonary molecular response of rats subjected to T/HS which did and did not develop lung injury as well as to non-shocked rats. Utilizing high-density oligonucleotide arrays and treatment group comparisons of whole lung tissue collected at 3 hours after the end of the shock or sham-shock period, 139 of the 8,799 assessed genes were differentially expressed. Experiment Overall Design: Four groups of rats (n=3) were studied in order to identify changes in pulmonary gene expression associated with T/HS, both in the presence and absence of lung injury. These included trauma-sham shock (T/SS) rats which had a laparotomy (trauma) but were not subjected to hemorrhagic shock. These rats had no lung injury and served as controls for rats which were subjected to T/HS (laparotomy plus 90 min of shock) and had lung injury. Differences in gene expression between these two groups would represent both the effects of hemorrhagic shock as well as lung injury. To distinguish the gene response of hemorrhagic shock from the gene response associated with lung injury, gene expression was also compared between T/HS rats (hemorrhage and lung injury) and rats subjected to T/HS plus lymph duct ligation (T/HS-LDL), since the T/HS-LDL rats experienced hemorrhagic shock but had no measurable lung injury. Lastly, to identify hemorrhagic shock- modified genes, the pulmonary gene response of T/HS-LDL (hemorrhage without lung injury) were compared to rats subjected to T/SS plus LDL (no hemorrhage or lung injury). Three hours after the end of the 90 min shock or sham-shock period (i.e. 4.5 hrs after the induction of T/HS), the rats were sacrificed and specimens harvested for genechip analysis and histology.
2008-06-14 | E-GEOD-6332 | biostudies-arrayexpress
Project description:CD39 or NTPDase1 and other nucleoside triphosphate diphosphohydrolases (NTPDases), including NTPDase2, NTPDase3, and NTPDase8, regulate purinergic signaling through tuning the extracellular levels of purine nucleotides and nucleosides. Purinergic signaling can regulate liver ischemia-reperfusion (I/R) injury and CD39 is protective. However, the role of other NTPDases is unkown. In this study, we have investigated the roles of NTPDase2, NTPDase3, and NTPDase8 in liver I/R injury. Global Entpd2-/-, Entpd3-/-, and Entpd8-/- and control wild-type (WT) mice were subjected to a 60 minutes of warm hepatic ischemia, which was followed by a 6-hour reperfusion period. In addition, WT and Entpd8-/- mice underwent global ischemia induced by hemorrhagic shock and resuscitation. Liver and plasma samples were collected to assess the extent and mechanisms of liver injury. Bone marrow chimeric mice derived from Entpd8-/- and WT were generated to understand the role of NTPDase expression on hematopoietic cells in regulating liver injury. While wild-type (WT), Entpd2-/- and Entpd3-/- mice exhibited comparable levels of liver injury following local IR, Entpd8-/- mice had increased liver injury compared to WT mice. This was evidenced by increased levels of plasma transaminases (ALT and AST) and histological evidence of heightened hepatocellular damage. Studies with bone marrow chimeric mice indicated that NTPDase8 on parenchymal liver cells protected against hepatic injury. This was confirmed by single-nucleus RNAseq showing hepatocytes are the dominant cell type expressing NTPDase8 in the liver. Entpd8-/- mice after I/R injury were noted to have higher ATP concentrations in the liver and plasma. The P2 antagonist suramin decreased plasma ALT and AST levels in Entpd8-/- mice indicating that extracellular ATP-mediated purinergic signaling contributes to liver injury in these mice. Finally, Entpd8-/- mice had increased liver injury compared to WT mice also after global IR induced by hemorrhagic shock and resuscitation.These findings highlight the differential roles of NTPDase family members in the liver, with parenchymal/hepatocyte expression of NTPDase8 emerging as a critical suppressor of the inflammatory and metabolic responses to hepatic ischemia-reperfusion insult, even in the presence of vascular NTPDase1 expression.
2025-12-30 | GSE280987 | GEO
Project description:Dengue viruses cause two severe diseases that alter vascular fluid barrier functions, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). While the mechanisms that lead to vascular permeability are unknown, the endothelium plays a central role in regulating fluid and cellular efflux from capillaries. Thus, dysregulation of endothelial cells functions by dengue virus infection may contribute to pathogenesis and severe disease. We used microarrays to investigate the effect of dengue virus infection on gene expression within primary human endothelial cells at various times post infection and identified numerous upregulated antiviral and immune response genes.
2012-04-11 | GSE34628 | GEO