Cyclooxygenase-1 and prostacyclin production by endothelial cells in the presence of mild oxidative stress.

This study aimed at evaluating the relative contribution of endothelial cyclooxygenase-1 and -2 (COX-1 and COX-2) to prostacyclin (PGI(2)) production in the presence of mild oxidative stress resulting from autooxidation of polyphenols such as (-)-epigallocatechin 3-gallate (EGCG), using both endothe...

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Autores principales:	Alice Toniolo, Carola Buccellati, Christian Pinna, Rosa Maria Gaion, Angelo Sala, Chiara Bolego
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f9a8c220c0674b58af6424291d824253
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spelling	oai:doaj.org-article:f9a8c220c0674b58af6424291d8242532021-11-18T07:57:08ZCyclooxygenase-1 and prostacyclin production by endothelial cells in the presence of mild oxidative stress.1932-620310.1371/journal.pone.0056683https://doaj.org/article/f9a8c220c0674b58af6424291d8242532013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23441213/?tool=EBIhttps://doaj.org/toc/1932-6203This study aimed at evaluating the relative contribution of endothelial cyclooxygenase-1 and -2 (COX-1 and COX-2) to prostacyclin (PGI(2)) production in the presence of mild oxidative stress resulting from autooxidation of polyphenols such as (-)-epigallocatechin 3-gallate (EGCG), using both endothelial cells in culture and isolated blood vessels. EGCG treatment resulted in an increase in hydrogen peroxide formation in human umbilical vein endothelial cells. In the presence of exogenous arachidonic acid and EGCG, PGI(2) production was preferentially inhibited by a selective COX-1 inhibitor. This effect of selective inhibition was also substantially reversed by catalase. In addition, EGCG caused vasorelaxation of rat aortic ring only partially abolished by a nitric oxide synthase inhibitor. Concomitant treatment with a selective COX-1 inhibitor completely prevented the vasorelaxation as well as the increase in PGI(2) accumulation in the perfusate observed in EGCG-treated aortic rings, while a selective COX-2 inhibitor was completely uneffective. Our data strongly support the notions that H(2)O(2) generation affects endothelial PGI(2) production, making COX-1, and not COX-2, the main source of endothelial PGI(2) under altered oxidative tone conditions. These results might be relevant to the reappraisal of the impact of COX inhibitors on vascular PGI(2) production in patients undergoing significant oxidative stress.Alice TonioloCarola BuccellatiChristian PinnaRosa Maria GaionAngelo SalaChiara BolegoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 2, p e56683 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Alice Toniolo Carola Buccellati Christian Pinna Rosa Maria Gaion Angelo Sala Chiara Bolego Cyclooxygenase-1 and prostacyclin production by endothelial cells in the presence of mild oxidative stress.
description	This study aimed at evaluating the relative contribution of endothelial cyclooxygenase-1 and -2 (COX-1 and COX-2) to prostacyclin (PGI(2)) production in the presence of mild oxidative stress resulting from autooxidation of polyphenols such as (-)-epigallocatechin 3-gallate (EGCG), using both endothelial cells in culture and isolated blood vessels. EGCG treatment resulted in an increase in hydrogen peroxide formation in human umbilical vein endothelial cells. In the presence of exogenous arachidonic acid and EGCG, PGI(2) production was preferentially inhibited by a selective COX-1 inhibitor. This effect of selective inhibition was also substantially reversed by catalase. In addition, EGCG caused vasorelaxation of rat aortic ring only partially abolished by a nitric oxide synthase inhibitor. Concomitant treatment with a selective COX-1 inhibitor completely prevented the vasorelaxation as well as the increase in PGI(2) accumulation in the perfusate observed in EGCG-treated aortic rings, while a selective COX-2 inhibitor was completely uneffective. Our data strongly support the notions that H(2)O(2) generation affects endothelial PGI(2) production, making COX-1, and not COX-2, the main source of endothelial PGI(2) under altered oxidative tone conditions. These results might be relevant to the reappraisal of the impact of COX inhibitors on vascular PGI(2) production in patients undergoing significant oxidative stress.
format	article
author	Alice Toniolo Carola Buccellati Christian Pinna Rosa Maria Gaion Angelo Sala Chiara Bolego
author_facet	Alice Toniolo Carola Buccellati Christian Pinna Rosa Maria Gaion Angelo Sala Chiara Bolego
author_sort	Alice Toniolo
title	Cyclooxygenase-1 and prostacyclin production by endothelial cells in the presence of mild oxidative stress.
title_short	Cyclooxygenase-1 and prostacyclin production by endothelial cells in the presence of mild oxidative stress.
title_full	Cyclooxygenase-1 and prostacyclin production by endothelial cells in the presence of mild oxidative stress.
title_fullStr	Cyclooxygenase-1 and prostacyclin production by endothelial cells in the presence of mild oxidative stress.
title_full_unstemmed	Cyclooxygenase-1 and prostacyclin production by endothelial cells in the presence of mild oxidative stress.
title_sort	cyclooxygenase-1 and prostacyclin production by endothelial cells in the presence of mild oxidative stress.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/f9a8c220c0674b58af6424291d824253
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Cyclooxygenase-1 and prostacyclin production by endothelial cells in the presence of mild oxidative stress.

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