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http://purl.uniprot.org/citations/17683945http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17683945http://www.w3.org/2000/01/rdf-schema#comment"

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Multiple pro-inflammatory mediators contribute to cardiac dysfunction caused by bacterial lipopolysaccharide (LPS). The rapid TNF-alpha response is likely involved in the induction of down-stream myocardial depressant factors. Studies by our laboratory and others indicate an important role for ICAM-1 in endotoxemic cardiac dysfunction through leukocyte-independent mechanisms. The purpose of this study was to determine: whether ICAM-1 knockout improves cardiac function during endotoxemia and whether TLR4 and TNF-alpha regulate LPS-induced myocardial ICAM-1 expression.

Methods and results

Mice were treated with Escherichia coli LPS (0.5mg/kg iv). Myocardial ICAM-1 levels were analyzed by immunoblotting and left ventricular developed pressure (LVDP) was assessed by the Langendorff technique. In wild-type mice, peak ICAM-1 levels were observed at 4h when myocardial contractility was depressed. Myocardial contractility was improved following LPS in mice lacking functional TLR4, TNF-alpha or ICAM-1. TLR4 mutation abolished ICAM-1 expression with abrogation of precedent TNF-alpha response. Similarly, TNF-alpha knockout reduced myocardial ICAM-1 level following LPS treatment.

Conclusions

ICAM-1 contributes to the mechanism of endotoxemic cardiac dysfunction. TNF-alpha is involved in the regulation of myocardial ICAM-1 expression by TLR4."xsd:string
http://purl.uniprot.org/citations/17683945http://purl.org/dc/terms/identifier"doi:10.1016/j.cyto.2007.05.018"xsd:string
http://purl.uniprot.org/citations/17683945http://purl.uniprot.org/core/author"Song Y."xsd:string
http://purl.uniprot.org/citations/17683945http://purl.uniprot.org/core/author"Meng X."xsd:string
http://purl.uniprot.org/citations/17683945http://purl.uniprot.org/core/author"Dinarello C.A."xsd:string
http://purl.uniprot.org/citations/17683945http://purl.uniprot.org/core/author"Ao L."xsd:string
http://purl.uniprot.org/citations/17683945http://purl.uniprot.org/core/author"Fullerton D.A."xsd:string
http://purl.uniprot.org/citations/17683945http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17683945http://purl.uniprot.org/core/name"Cytokine"xsd:string
http://purl.uniprot.org/citations/17683945http://purl.uniprot.org/core/pages"124-129"xsd:string
http://purl.uniprot.org/citations/17683945http://purl.uniprot.org/core/title"The interaction between myocardial depressant factors in endotoxemic cardiac dysfunction: role of TNF-alpha in TLR4-mediated ICAM-1 expression."xsd:string
http://purl.uniprot.org/citations/17683945http://purl.uniprot.org/core/volume"38"xsd:string
http://purl.uniprot.org/citations/17683945http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17683945
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