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• W1982251171 startingPage "42619" @default.
• W1982251171 abstract "Proinflammatory cytokines have been linked to depression of myocardial contractility in vivo in patients with acute septic shock and in vitro models employing isolated myocytes exposed to serum from such patients. The key pathways involved in mediating this septic organ dysfunction (cell adhesion molecule expression, inducible nitric-oxide synthase induction, and apoptosis) are known to be regulated by transcription factors STAT1, IRF1, and NF-kappaB. Utilizing a model that mimics human disease, we have demonstrated activation of the transcription factors STAT1, IRF1, and NF-kappaB in human fetal myocytes exposed to human septic serum. Both reporter and electrophoretic mobility shift assays demonstrated a 5-19-fold increase in activation of transcription factors STAT1, IRF1, and NF-kappaB in response to incubation with human septic serum. The addition of human septic serum to human fetal myocytes induced apoptosis in human fetal myocytes and activation of the mitogen-activated protein kinase c-Jun NH -terminal kinase and caspase 1 as measured by Western blot. These data suggest that transcription factor activation and early myocyte apoptosis play a mechanistic role in septic myocardial depression and sepsis-induced organ dysfunction." @default.
• W1982251171 created "2016-06-24" @default.
• W1982251171 creator A5005349109 @default.
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• W1982251171 date "2005-12-01" @default.
• W1982251171 modified "2023-10-18" @default.
• W1982251171 title "Human Serum from Patients with Septic Shock Activates Transcription Factors STAT1, IRF1, and NF-κB and Induces Apoptosis in Human Cardiac Myocytes" @default.
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• W1982251171 doi "https://doi.org/10.1074/jbc.m508416200" @default.
• W1982251171 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16223733" @default.
• W1982251171 hasPublicationYear "2005" @default.
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