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- W2071464503 abstract "Objective: Blood levels of cytokines are commonly elevated in severe congestive heart failure (CHF) and in coronary artery disease (CAD). While the adverse effects of cytokines on contractile function and myocardial cell integrity are well studied, little is known on whether cardiac cells are only targets or active players in these inflammatory reactions. Methods and results: We tested if human coronary artery endothelial cells (HCAEC) may become a source of cytokine and adhesion molecule expression when stimulated with bacterial lipopolysaccharide (LPS). Analysis of HCAEC supernatants by ELISA identified enhanced secretion of IL-6, IL-8, and MCP-1 while endothelin-1 was not increased. IL-1β, IL-10, or TNF-α were not detectable by ELISA while RT-PCR revealed enhanced mRNA expression of IL-1β and TNF-α but not IL-10. FACS analysis showed an LPS-induced upregulation of ICAM-1, VCAM, and ELAM-1. LFA-1 could not be detected. We further characterized receptors involved in LPS-induced signaling. Our results indicate that activation of HCAEC by LPS requires Toll-like receptor (TLR) 4. Pretreating the cells with the 3-hydroxy-3-methylglutaryl CoA (HMG CoA) reductase inhibitor Cerivastatin reduced IL-6 release. Conclusions: Taken together, our results indicate that activated HCAEC may act as inflammatory cells and thus directly contribute to the progression of CHF and CAD." @default.
- W2071464503 created "2016-06-24" @default.
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- W2071464503 date "2002-10-01" @default.
- W2071464503 modified "2023-10-12" @default.
- W2071464503 title "TLR4-mediated inflammatory activation of human coronary artery endothelial cells by LPS" @default.
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- W2071464503 doi "https://doi.org/10.1016/s0008-6363(02)00512-6" @default.
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