dc.creatorde Oliveira-Junior, EB
dc.creatorThomazzi, SM
dc.creatorRelider, J
dc.creatorAntunes, E
dc.creatorCondino-Neto, A
dc.date2007
dc.date41091
dc.date2014-11-18T16:30:16Z
dc.date2015-11-26T16:57:18Z
dc.date2014-11-18T16:30:16Z
dc.date2015-11-26T16:57:18Z
dc.date.accessioned2018-03-28T23:44:51Z
dc.date.available2018-03-28T23:44:51Z
dc.identifierEuropean Journal Of Pharmacology. Elsevier Science Bv, v. 567, n. 41671, n. 43, n. 49, 2007.
dc.identifier0014-2999
dc.identifierWOS:000247281700006
dc.identifier10.1016/j.ejphar.2007.04.018
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/64091
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/64091
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/64091
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1277627
dc.descriptionWe investigated the effects of the 5-cyclopropyl-2-[1-(2-fluoro-benzyl)-1H-pyrazolo[3,4-b] pyridin-3-yl]-pyrimidin-4-ylamine (BAY 41-2272) on the NADPH oxidase activity, gp91(phox) gene expression, cyclic guanosine-3',5-monophosphate (cGMP) and cyclic adenosine-3',5'-monophosphate (cAMP) levels in the human myelomonocytic THP-1 cell line. THP-1 cells treated with BAY 41-2272 (0.3-10 mu M) for 48 h significantly increased the superoxide anion (O-2(center dot-)) release. This increase was not affected when cells were pre-treated with the specific cGMP-phosphodiesterase inhibitor zaprinast, the soluble guanylate cyclase inhibitor 1H-[1,2,4] oxidiazolo[4,3-alpha] quinoxalin-1-one (ODQ), the adenylate cyclase inhibitor 9-(tetrahydro-2-furanyl) adenine (SQ 22,536) or the nitric oxide synthase inhibitor N-omega-nitro-1-arginine methyl ester (I-NAME). In addition, BAY 41-2272 (3 and 10 mu M; 48 h) was able to increase gp91(phox) gene expression on THP-1 cells. The pre-treatment with zaprinast, 3-isobutyl-L-methyl-xanthine (IBMX; 0.5 mM), ODQ, SQ 22,536 or l-NAME caused no additional effect on the expression of gp91(phox) evoked by BAY 41-2272. Treatment of THP-1 cells with BAY 41-2272 caused a significant increase in cGMP and cAMP levels. Our findings show that BAY 41-2272 caused a significant increase on the O-2(center dot-) release and gp91(phox) gene expression by THP-1 cells, and an elevation of intracellular cGMP and cAMP levels. However, we could not detect a clear correlation between both O-2(center dot-) release and gp91(phox) gene expression with activation of cGMP and cAMP signaling pathways. (c) 2007 Elsevier B.V. All rights reserved.
dc.description567
dc.description41671
dc.description43
dc.description49
dc.languageen
dc.publisherElsevier Science Bv
dc.publisherAmsterdam
dc.publisherHolanda
dc.relationEuropean Journal Of Pharmacology
dc.relationEur. J. Pharmacol.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectBAY 41-2272
dc.subjectcAMP
dc.subjectcGMP
dc.subjectgp91(phox)
dc.subjecthuman macrophage
dc.subjectmyeloid cell
dc.subjectNADPH oxidase
dc.subjectphagocyte
dc.subjectAdenosine 3'-5'-monophosphate-inducing Agents
dc.subjectChronic Granulomatous-disease
dc.subjectPig Pulmonary-artery
dc.subjectInduced-differentiation
dc.subjectGp91(phox) Expression
dc.subjectMolecular-mechanisms
dc.subjectSuperoxide Formation
dc.subjectEnzyme Immunoassays
dc.subjectEndothelial-cells
dc.subjectMononuclear-cells
dc.titleEffects of BAY 41-2272, an activator of nitric oxide-independent site of soluble guanylate cyclase, on human NADPH oxidase system from THP-1 cells
dc.typeArtículos de revistas


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