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)

The expression of a cytoskeletal protein, beta-actin, mRNA was examined in hypothermic ischemic brains. Mongolian gerbils were subjected to forebrain ischemia by bilateral carotid occlusion of 10 min at 30 degrees C followed by normothermic reperfusion for 1 h or 6 h, 1 day or 3 days, 2 weeks or 1 month. The expression of beta-actin mRNA was determined in hypothermic controls and postischemic (PI) animals subjected to intra-ischemic hypothermia using in situ hybridization. On comparing the pattern of expression of beta-actin in hypothermic ischemic brains with that in normothermic ischemic brains, it was noted that there was no significant decline in its expression in the CA1 region of hypothermic ischemic brains as noted in the normothermic ischemic brains (reported by us previously). Only one hypothermic ischemic animal in the 2 week PI period showed marked reduction in its expression in the CA1 region. These results indicate that hypothermia leads to preservation of the expression of a cytoskeletal protein, beta-actin, in a selectively vulnerable region of the brain following ischemia.
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PMID:Hypothermia preserves expression of beta-actin mRNA in ischemic brain. 874 75

The transition from reversible to irreversible ischemic injury (ischemia-reperfusion, I/R) occurs coincident with the loss of vinculin, a cytoskeletal protein involved in the attachment of the myofibrils to the sarcolemmal membrane. If the loss of vinculin were critical to the development of I/R, then increased levels of vinculin would be predicted to delay the onset of irreversible injury assuming that the protein is functional and localized to the proper subcellular site. The present study determined whether increased expression of vinculin, specifically in the cytoskeletal compartment, would provide protection from I/R injury. Neonatal rat myocytes were cultured and infected with a newly created replication-deficient adenovirus driving the expression of vinculin. I/R was induced with chemical inhibitors of glycolysis and mitochondrial respiration. Irreversible cell injury was assessed with lactate dehydrogenase (LDH) release. Virus-infected myocytes expressed significantly more vinculin in the cytoskeletal fraction and increased the expression of paxillin but sustained the same amount of injury in response to simulated I/R as control cells (n = 4; P = not significant, paired t-test). Hypothermic I/R (ischemia at 25 degrees C) resulted in a significant reduction in LDH release (P </= 0.02; n = 4). Virus-mediated overexpression of vinculin does not appear to represent a rational approach to overcoming I/R injury.
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PMID:Effect of increased expression of cytoskeletal protein vinculin on ischemia-reperfusion injury in ventricular myocytes. 1257 17