Abstract
This study is focused on the links between the major products of inflammation and cell damage induced by the administration of lipopolysaccharide (LPS) from Salmonella typhimurium in embryonal cardiomyocytes. LPS treatment for 72 hours induced transcription factor NF-κB activation, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 expression, nitric oxide (NO) and tumor necrosis factor (TNF)-α release. Moreover, LPS administration induced a significant cell loss, reversed by the NO-synthases inhibitor, suggesting a relationship between cell damage and iNOS-dependent NO overproduction. Cell death was reversed by the specific NF-κB inhibitor, TPCK, whereas COX-2 specific inhibitor determined an increase of cell damage in terms of apoptosis, as observed by YO-PRO immunostaining, DNA laddering analysis and caspase-3 activation. Overall these findings evidenced a selective role for NF-κB in mediating NO-induced cell damage and a protective action by COX-2 in LPS-treated embryonal cardiomyocytes. The reflection of these experiments on human cardiac pathology will be discussed.
Keywords: LPS, chick embryo, cardiomyocyte, NF-κB, nitric oxide, COX-2, apoptosis
Current Pharmaceutical Design
Title: Inflammatory Responses in Embryonal Cardiomyocytes Exposed to LPS Challenge. An In Vitro Model of Deciphering the Effects of LPS on the Heart
Volume: 16 Issue: 7
Author(s): Maria Antonietta Panaro, Angela Acquafredda, Pasqua Cavallo, Antonia Cianciulli, Concetta Saponaro and Vincenzo Mitolo
Affiliation:
Keywords: LPS, chick embryo, cardiomyocyte, NF-κB, nitric oxide, COX-2, apoptosis
Abstract: This study is focused on the links between the major products of inflammation and cell damage induced by the administration of lipopolysaccharide (LPS) from Salmonella typhimurium in embryonal cardiomyocytes. LPS treatment for 72 hours induced transcription factor NF-κB activation, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 expression, nitric oxide (NO) and tumor necrosis factor (TNF)-α release. Moreover, LPS administration induced a significant cell loss, reversed by the NO-synthases inhibitor, suggesting a relationship between cell damage and iNOS-dependent NO overproduction. Cell death was reversed by the specific NF-κB inhibitor, TPCK, whereas COX-2 specific inhibitor determined an increase of cell damage in terms of apoptosis, as observed by YO-PRO immunostaining, DNA laddering analysis and caspase-3 activation. Overall these findings evidenced a selective role for NF-κB in mediating NO-induced cell damage and a protective action by COX-2 in LPS-treated embryonal cardiomyocytes. The reflection of these experiments on human cardiac pathology will be discussed.
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Cite this article as:
Panaro Antonietta Maria, Acquafredda Angela, Cavallo Pasqua, Cianciulli Antonia, Saponaro Concetta and Mitolo Vincenzo, Inflammatory Responses in Embryonal Cardiomyocytes Exposed to LPS Challenge. An In Vitro Model of Deciphering the Effects of LPS on the Heart, Current Pharmaceutical Design 2010; 16 (7) . https://dx.doi.org/10.2174/138161210790883516
DOI https://dx.doi.org/10.2174/138161210790883516 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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