Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mild hypothermia protects against neuronal damage after transient global ischemia in experimental animals. The exact mechanism of this protective effect remains to be elucidated. The purpose of the present study was to investigate the molecular mechanisms relevant to different neurologic responses to hypothermia and normothermia. Transient global ischemia was induced in C57BL/6 mice by bilateral common carotid artery occlusion for 10 min. Hypothermia provided robust neuroprotection in the hippocampus region and dramatically reduced the mortality rate. Using adaptor-tagged competitive polymerase chain reaction, we obtained the relative transcription levels of 1210 genes in the hippocampal region and compared the expression patterns of these genes. Two genes, Activity-regulated cytoskeleton-associated protein (Arc) and CUG-binding protein-2 (Cugbp2), showed remarkable and persistent increases in their expression levels in normothermic mice, compared with in both sham and hypothermic mice. Despite the increased transcription of Arc and Cugbp2, an immunohistochemistry analysis did not show comparable increases in the translations of both genes. Only a transient increase in Arc protein was observed in the granule cells of the dentate gyrus at 6 h after reperfusion. A remarkable decrease in Cugbp2 protein was observed in the pyramidal cells of the hippocampal CA1-CA3, in accordance with the progress of neuronal degeneration. A decrease in Cugbp2 protein was not observed in hypothermic mice. These results suggest that transient global ischemia induces the translational inhibition of genes with increased expression not in hypothermic, but in normothermic mice. Thus, translational inhibition might play an important role in the progress of neuronal injury after transient global ischemia.
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PMID:Transcriptional induction and translational inhibition of Arc and Cugbp2 in mice hippocampus after transient global ischemia under normothermic condition. 1955 13

Though important for a variety of medical procedures, general anesthesia is not a problem free. Some anesthetics have been suggested to affect a number of signals, which are associated with memory consolidation and cognition. In the present study, we attempted to investigate the molecular mechanism of anesthesia-regulated processes. We found that under hypothermic condition, anesthetic of isoflurane enhances various signals expression in hippocampus, including Hspd1, Actb, Mgst1, THBS4, Syp, C1QC, Serpine, Plat, and Ngf, which were related to cellular stress, neural plasticity responses, and hippocampal injury. Importantly, isoflurane and propofol anesthesia reduced fibroblast growth factor (FGF2) and activity-regulated cytoskeleton-associated protein (Arc) expressions, enhanced glial fibrillary acidic protein (GFAP), Iba1 and phosphorylated-Eukaryotic elongation factor 2 (eEF2) levels as well as down-regulated mitogen-activated protein kinases (MAPKs) family members, including p38, ERK1/2 and JNK, in the hippocampus of animals. Moreover, the in vivo cold water swimming (CWS) experiment and in vitro hypothermic incubation of cells further confirmed our hypothesis that hypothermia is tightly linked to the reduction of FGF2 and Arc, augment of GFAP, Iba1 and p-eEF2, and the decreasing of MAPKs. Generally, our study provided new insights into the modulation of various signals by anesthesia-triggered hypothermia.
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PMID:Hypothermia induced by anesthesia regulates various signals expressions in the hippocampus of animals. 2893 23