Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/48295
DC FieldValueLanguage
dc.contributor.authorTabraue, Carlosen_US
dc.contributor.authorDiaz Peñate, Raquelen_US
dc.contributor.authorGallardo, Germanen_US
dc.contributor.authorHernandez Gonzalez, Inmaculadaen_US
dc.contributor.authorQuintana, Joséen_US
dc.contributor.authorLópez Blanco, Felixen_US
dc.contributor.authorGonzález Reyes, Juanen_US
dc.contributor.authorFanjul, Luisa F.en_US
dc.contributor.authorRuiz De Galarreta, Carlos M.en_US
dc.contributor.otherQuintana, Jose-
dc.contributor.otherTabraue, Carlos-
dc.date.accessioned2018-11-23T20:30:43Z-
dc.date.available2018-11-23T20:30:43Z-
dc.date.issued1997en_US
dc.identifier.issn0013-7227en_US
dc.identifier.urihttp://hdl.handle.net/10553/48295-
dc.description.abstractIn cultured granulosa cells, interleukin-1β(IL-1β) induced a time- dependent (16-72 h) and dose-related (0.3-30 ng/ml) stimulation of nitric oxide (NO) synthase (NOS) activity, as determined by the catalytic conversion of [3H]arginine to [3H]citrulline and NO2 accumulation in the culture medium. Although FSH alone failed to stimulate NOS activity, concomitant treatment with the gonadotropin (200 ng/ml) or the cell-permeant cAMP analog (Bu)2cAMP (0.5 mM) markedly enhanced IL-1β-induced NO generation in cultured granulosa cells. The effect of IL-1β on citrulline biosynthesis and NO2 accumulation was abrogated by the NOS inhibitor N(G)-methyl-L-arginine or the IL-1-receptor antagonist protein. In contrast bacterial endotoxin (lipopolysaccharide), interferon-γ or tumor necrosis factor-α, which are well known inducers of inducible NOS (iNOS) in a variety of immunocompetent and nonimmunocompetent cell types, failed to increase [3H]citrulline formation or NO2 accumulation in untreated or FSH-stimulated cells. As demonstrated by reverse transcriptase-PCR analysis, IL-1β-stimulated NO generation was accompanied by a time-dependent increase in messenger RNA levels for iNOS and GTP-cyclohydrolase (GTPCH), the rate-limiting step for de novo tetrahydrobiopterin (BH4) biosynthesis. Treatment with FSH augmented only GTPCH messenger RNA expression, and a more than additive GTPCH signal was observed when cells were simultaneously challenged with IL-1β and FSH. Treatment with the GTPCH inhibitor 2,4-diamino-6-hydroxypyrimidine prevented IL-1β-induced NOS activity in untreated or FSH-stimulated cells, and this inhibition was completely reversed by sepiapterin, a substrate for BH4 biosynthesis, via an alternative pterin salvage pathway present in many cell types. As BH4 is an essential cofactor for NOS catalytic activity, these observations strongly suggest that FSH-induced biosynthesis of endogenous BH4 is essential for full iNOS biosynthetic capacity in IL-1β-stimulated granulosa cells.en_US
dc.languageengen_US
dc.relation.ispartofEndocrinology (Philadelphia)en_US
dc.sourceEndocrinology [ISSN 0013-7227],v. 138 (1), p. 162-168en_US
dc.subject2403 Bioquímicaen_US
dc.subject320502 Endocrinologíaen_US
dc.subject2415 Biología molecularen_US
dc.subject32 Ciencias médicasen_US
dc.subject.otherVascular Smooth-Muscleen_US
dc.subject.otherRat Ovaryen_US
dc.subject.otherReceptor Antagonisten_US
dc.subject.otherMessenger-Rnaen_US
dc.subject.otherCytokinesen_US
dc.subject.otherTetrahydrobiopterinen_US
dc.subject.otherInterleukin-1en_US
dc.subject.otherExpressionen_US
dc.subject.otherInhibitionen_US
dc.subject.otherDifferentiationen_US
dc.titleInduction of guanosine triphosphate-cyclohydrolase by follicle- stimulating hormone enhances interleukin-1β-stimulated nitric oxide synthase activity in granulosa cellsen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1210/endo.138.1.4854en_US
dc.identifier.scopus0031014552-
dc.identifier.isiA1997VZ82400025-
dcterms.isPartOfEndocrinology-
dcterms.sourceEndocrinology[ISSN 0013-7227],v. 138 (1), p. 162-168-
dc.contributor.authorscopusid6506833060-
dc.contributor.authorscopusid6505605355-
dc.contributor.authorscopusid6603046608-
dc.contributor.authorscopusid57211220417-
dc.contributor.authorscopusid57211220417-
dc.contributor.authorscopusid8681043500-
dc.contributor.authorscopusid6602478628-
dc.contributor.authorscopusid6602478628-
dc.contributor.authorscopusid16167408800-
dc.contributor.authorscopusid7004158812-
dc.contributor.authorscopusid7003806034-
dc.description.lastpage168en_US
dc.identifier.issue1-
dc.description.firstpage162en_US
dc.relation.volume138en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.identifier.wosWOS:A1997VZ82400025-
dc.contributor.daisngid4816905-
dc.contributor.daisngid8838806-
dc.contributor.daisngid22271832-
dc.contributor.daisngid7801524-
dc.contributor.daisngid29513481-
dc.contributor.daisngid1412131-
dc.contributor.daisngid128315-
dc.contributor.daisngid2864371-
dc.contributor.daisngid369809-
dc.contributor.daisngid1127140-
dc.contributor.daisngid22434817-
dc.identifier.investigatorRIDK-5709-2014-
dc.identifier.investigatorRIDD-7126-2015-
dc.description.numberofpages7en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Tabraue, C-
dc.contributor.wosstandardWOS:Penate, RD-
dc.contributor.wosstandardWOS:Gallardo, G-
dc.contributor.wosstandardWOS:Hernandez, I-
dc.contributor.wosstandardWOS:Quintana, J-
dc.contributor.wosstandardWOS:Blanco, FL-
dc.contributor.wosstandardWOS:Reyes, JG-
dc.contributor.wosstandardWOS:Fanjul, LF-
dc.contributor.wosstandardWOS:DeGalarreta, GMR-
dc.date.coverdateEnero 1997en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.jcr4,348-
dc.description.jcrqQ1-
dc.description.scieSCIE-
item.grantfulltextnone-
item.fulltextSin texto completo-
crisitem.author.deptGIR Medio Ambiente y Salud-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Morfología-
crisitem.author.deptGIR Medio Ambiente y Salud-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Didácticas Específicas-
crisitem.author.deptGIR Señalización Intracelular y Expresión Génica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.deptGIR Bioquímica Farmacológica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.deptGIR Medio Ambiente y Salud-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.deptGIR Señalización Intracelular y Expresión Génica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.orcid0000-0001-9920-8116-
crisitem.author.orcid0000-0002-1516-1750-
crisitem.author.orcid0000-0001-8937-9034-
crisitem.author.orcid0000-0001-8225-4538-
crisitem.author.orcid0000-0003-1167-9787-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameTabraue Tarbay, Carlos-
crisitem.author.fullNameGallardo Campos, Germán-
crisitem.author.fullNameHernández González, Inmaculada Servanda-
crisitem.author.fullNameQuintana Aguiar, José Martín-
crisitem.author.fullNameLópez Blanco, Félix-
crisitem.author.fullNameFanjul Rodríguez, Luisa Fernanda-
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