Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/53526
DC FieldValueLanguage
dc.contributor.authorCabrera, J-
dc.contributor.authorQuintana, J-
dc.contributor.authorReiter, RJ-
dc.contributor.authorLoro, J-
dc.contributor.authorCabrera, F-
dc.contributor.authorEstevez, F-
dc.contributor.otherCabrera, Javier-
dc.contributor.otherQuintana, Jose-
dc.contributor.otherEstevez, Francisco-
dc.contributor.otherloro, juan-
dc.date.accessioned2019-02-04T17:03:12Z-
dc.date.available2019-02-04T17:03:12Z-
dc.date.issued2003-
dc.identifier.issn0742-3098-
dc.identifier.urihttp://hdl.handle.net/10553/48406-
dc.description.abstractPrevious studies have reported that melatonin protects cells and tissues against stressful stimuli. In the present study using HL-60 cells, we show that cells acquire increased resistance to apoptosis normally induced by heat shock when they are incubated with melatonin. This effect of melatonin is saturable at nanomolar concentrations and appears to be mediated by the MT2 subtype melatonin receptor. The high affinity melatonin receptor agonist, 2-iodomelatonin, reproduced the melatonin effect while it was fully blocked by the selective MT2 antagonist 4-phenyl-2-propionamidotetraline. The melatonin response to heat shock-induced apoptosis was pertussis toxin sensitive and, interestingly, the non-selective MT1/MT2 melatonin receptor ligand luzindole was found to display agonistic activity. Furthermore, we provide evidence that melatonin enhanced HSP27 mRNA expression as a result of heat shock - HSP27, is known to play an important role in the defense of cells against apoptosis induced by stressful agents. Together, these results demonstrate that melatonin, likely via receptor mechanisms, interferes with the apoptotic pathway activated by heat shock.-
dc.languageeng-
dc.publisher0742-3098-
dc.relation.ispartofJournal of Pineal Research-
dc.sourceJournal of Pineal Research[ISSN 0742-3098],v. 35, p. 231-238 (Noviembre 2003)-
dc.subject32 Ciencias médicas-
dc.subject.otherHyperthermia-Induced Apoptosis-
dc.subject.otherG-Protein-
dc.subject.otherIschemia-Reperfusion-
dc.subject.otherSignal-Transduction-
dc.subject.otherOxidative Damage-
dc.subject.otherCyclic-Amp-
dc.subject.otherDeath-
dc.subject.otherRats-
dc.subject.otherCeramide-
dc.subject.otherHeat-Shock-Protein-70-
dc.titleMelatonin prevents apoptosis and enhances HSP27 mRNA expression induced by heat shock in HL-60 cells: possible involvement of the MT2 receptor-
dc.typeinfo:eu-repo/semantics/Article-
dc.typeArticle-
dc.identifier.doi10.1034/j.1600-079X.2003.00071.x-
dc.identifier.scopus0242269986-
dc.identifier.isi000185679800002-
dcterms.isPartOfJournal Of Pineal Research-
dcterms.sourceJournal Of Pineal Research[ISSN 0742-3098],v. 35 (4), p. 231-238-
dc.contributor.authorscopusid35598975600-
dc.contributor.authorscopusid8681043500-
dc.contributor.authorscopusid7402574751-
dc.contributor.authorscopusid6507389169-
dc.contributor.authorscopusid57197219173-
dc.contributor.authorscopusid7003810011-
dc.description.lastpage238-
dc.identifier.issue4-
dc.description.firstpage231-
dc.relation.volume35-
dc.type2Artículo-
dc.identifier.wosWOS:000185679800002-
dc.contributor.daisngid240124-
dc.contributor.daisngid128315-
dc.contributor.daisngid227-
dc.contributor.daisngid3210878-
dc.contributor.daisngid2128761-
dc.contributor.daisngid2680482-
dc.contributor.daisngid384944-
dc.identifier.investigatorRIDL-9179-2014-
dc.identifier.investigatorRIDK-5709-2014-
dc.identifier.investigatorRIDK-5125-2014-
dc.identifier.investigatorRIDNo ID-
dc.description.numberofpages8-
dc.utils.revision-
dc.contributor.wosstandardWOS:Cabrera, J-
dc.contributor.wosstandardWOS:Quintana, J-
dc.contributor.wosstandardWOS:Reiter, RJ-
dc.contributor.wosstandardWOS:Loro, J-
dc.contributor.wosstandardWOS:Cabrera, F-
dc.contributor.wosstandardWOS:Estevez, F-
dc.date.coverdateNoviembre 2003-
dc.identifier.ulpgc-
dc.description.jcr3,426-
dc.description.jcrqQ1-
dc.description.scieSCIE-
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptGIR IUIBS: 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 IUIBS: Bioquímica Farmacológica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.deptGIR IUIBS: Bioquímica Farmacológica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.orcid0000-0001-8225-4538-
crisitem.author.orcid0000-0002-0517-8209-
crisitem.author.orcid0000-0002-9728-2774-
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.fullNameQuintana Aguiar, José Martín-
crisitem.author.fullNameLoro Ferrer, Juan Francisco-
crisitem.author.fullNameEstévez Rosas, Francisco Jesús-
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