Differential expression of nitric oxide synthases in porcine aortic endothelial cells during LPS-induced apoptosis
<p>Abstract</p> <p>Background</p> <p>It is well known that nitric oxide (NO) is generated by a family of constitutively (nNOS and eNOS) or inducibly (iNOS) expressed enzymes and takes part in different aspects of the inflammatory response; nevertheless, its effective ro...
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2012-11-01T00:00:00Z.
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LEADER | 00000 am a22000003u 4500 | ||
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001 | doaj_4bd77200978c4fe6b0fb653250a3bcf4 | ||
042 | |a dc | ||
100 | 1 | 0 | |a Bernardini Chiara |e author |
700 | 1 | 0 | |a Greco Francesca |e author |
700 | 1 | 0 | |a Zannoni Augusta |e author |
700 | 1 | 0 | |a Bacci Maria Laura |e author |
700 | 1 | 0 | |a Seren Eraldo |e author |
700 | 1 | 0 | |a Forni Monica |e author |
245 | 0 | 0 | |a Differential expression of nitric oxide synthases in porcine aortic endothelial cells during LPS-induced apoptosis |
260 | |b BMC, |c 2012-11-01T00:00:00Z. | ||
500 | |a 10.1186/1476-9255-9-47 | ||
500 | |a 1476-9255 | ||
520 | |a <p>Abstract</p> <p>Background</p> <p>It is well known that nitric oxide (NO) is generated by a family of constitutively (nNOS and eNOS) or inducibly (iNOS) expressed enzymes and takes part in different aspects of the inflammatory response; nevertheless, its effective role in the pathogenesis of multiple organ dysfunction and septic shock is not fully understood.</p> <p>Methods</p> <p>To investigate the Nitric Oxide Synthases (NOSs) expression in endothelial cells during endotoxin exposure and the involvement of NO in lipopolysaccharide (LPS)-induced apoptosis, primary cultures of porcine Aortic Endothelial Cells (pAECs) were exposed to LPS for different time periods (1-24 h) and to LPS + L-NAME (15 h).</p> <p>Results</p> <p>Lipopolysaccharide induced an increase in mRNA and protein iNOS expression; on the contrary, the expression of eNOS was decreased. Furthermore, NOSs localisation was in part modified by LPS treatment. No alteration in the total level of Nitric Oxide was observed. L-NAME (5 mM) addition determined a slight decrease of LPS-induced apoptosis.</p> <p>Conclusions</p> <p>Endotoxin treatment strongly influenced NOS expression with an upregulation of iNOS and a simultaneous down regulation of eNOS. Moreover, in our model, the involvement of NO on LPS-induced apoptosis is very modest, suggesting that different pathways are involved in the regulation of this process.</p> | ||
546 | |a EN | ||
690 | |a Endothelial cells | ||
690 | |a Endotoxin | ||
690 | |a Apoptosis | ||
690 | |a NO | ||
690 | |a Therapeutics. Pharmacology | ||
690 | |a RM1-950 | ||
655 | 7 | |a article |2 local | |
786 | 0 | |n Journal of Inflammation, Vol 9, Iss 1, p 47 (2012) | |
787 | 0 | |n http://www.journal-inflammation.com/content/9/1/47 | |
787 | 0 | |n https://doaj.org/toc/1476-9255 | |
856 | 4 | 1 | |u https://doaj.org/article/4bd77200978c4fe6b0fb653250a3bcf4 |z Connect to this object online. |