Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tissue factor (TF) triggers the coagulation cascade reaction in vivo. Overexpression of TF mRNA is one leading cause of disseminated intravascular coagulation and thrombosis-related organ failure. In response to lipopolysaccharide (LPS) stimulation, various cell types can produce TF mRNA in vitro. However, there is currently no agreement on what types of cells in the liver overexpress TF mRNA after LPS treatment. For the first report, we found the increased TF mRNA with reverse transcription-polymerase chain reaction (RT-PCR), and confirmed a fourfold increase (p<0.001 vs. control, t-test) of the TF mRNA level with RT-competitive PCR in the liver of LPS-treated (2.0 mg/kg i.v. injection) rats. There was no significant difference in the glyceraldehyde-3-phosphate dehydrogenase mRNA level between LPS-treated rats and control rats. To clarify the localization and cellular source of LPS-induced TF mRNA, we performed in situ hybridization analysis with [35S]-labeled oligonucleotides probes, which we originally designed. We detected intense signals of TF mRNA in mononuclear cells but not in endothelial cells around the hepatic vein of LPS-treated rats. In this study, we showed that the TF mRNA level induced by LPS treatment, which may indicate mononuclear cells associated, significantly increased in the liver of rats. These results will provide circumstantial support for the therapeutic strategy that mononuclear cell should be one of the target cells to be treated in the early phase of disseminated intravascular coagulation in the liver, and that the need to suppress its overexpression of TF mRNA is essential for preventing hypercoagulable condition.
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PMID:Detection of mononuclear cells as the source of the increased tissue factor mRNA in the liver from lipopolysaccharide-treated rats. 1068 Jun 46

Oxidative stress results from an oxidant/antioxidant imbalance, an excess of oxidants and/or a depletion of antioxidants. A considerable body of recent evidence suggests that oxidant stress plays a major role in several aspects of septic shock and disseminated intravascular coagulation (DIC), and it is the subject of this review. Immunohistochemical and biochemical evidence demonstrate the significant role of reactive oxygen species (ROS) in endotoxic and hemorrhagic shock, and in endothelial injury associated with DIC syndrome. Initiation of lipid peroxidation, direct inhibition of mitochondrial respiratory chain enzymes, inactivation of glyceraldehyde-3-phosphate dehydrogenase, inhibition of membrane Na+/K+ ATP-ase activity, inactivation of membrane sodium channels, and other oxidative protein modifications contribute to the cytotoxic effect of ROS. In addition, reactive oxygen species are potent triggers of DNA strand breakage, with subsequent activation of the nuclear enzyme poly-ADP ribosyl synthetase, with eventual severe energy depletion of the cells. Pharmacological evidence suggests that the peroxynitrite-poly-ADP ribosyl synthetase pathway contributes to the cellular injury in shock and endothelial injury. Treatment with superoxide dismutase mimetics (SODms), which selectively mimic the catalytic activity of the human superoxide dismutase enzymes, have been shown to prevent in vivo shock and the cellular energetic failure associated with shock.
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PMID:Oxidative stress in septic shock and disseminated intravascular coagulation. 1239 25