Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/49318
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dc.contributor.authorRodriguez-Esparragon, Franciscoen_US
dc.contributor.authorSerna-Gómez, Jaime Albertoen_US
dc.contributor.authorHernández-Velázquez, Érikaen_US
dc.contributor.authorBuset-Ríos, Nisaen_US
dc.contributor.authorHernández-Trujillo, Yaridéen_US
dc.contributor.authorGarcía-Bello, Miguel A.en_US
dc.contributor.authorRodriguez-Perez, Jose C.en_US
dc.contributor.otherRodriguez-Esparragon, Francisco-
dc.contributor.otherRodriguez-Perez, J.C.-
dc.contributor.otherGarcia-Bello, Miguel-Angel-
dc.date.accessioned2018-11-24T06:12:53Z-
dc.date.available2018-11-24T06:12:53Z-
dc.date.issued2012en_US
dc.identifier.issn0300-8177en_US
dc.identifier.urihttp://hdl.handle.net/10553/49318-
dc.description.abstractThe resistance of internal mammary artery (IMA) toward atherosclerosis is not well understood. In plasma, homocysteine (Hcy) occurs in reduced, oxidized, homocysteine thiolactone and a component of proteins as a result of N- or S-homocysteinylation. We evaluated S/N-homocysteinylated protein levels in IMA fragments of patients undergoing coronary artery bypass grafting, and whether they were affected by genetic common variants. We tested whether tHcy, Hcy-S-protein levels, genotypes or Hcy-induced methylation modifications were related to differences in iNOS, Ddah2, and eNOS gene expression between territories. A small percentage of Hcy-S-proteins were found in IMA fragments. The Mthfr C677T (rs1801133) and Pon-1 Leu55Met (rs854560) variants were associated with Hcy-S-proteins. We observed a gradual difference according to Hcy-S-protein levels in the methylation degree of the Ddah2 gene promoter in aortic, but not in IMA, fragments. No correlation between the degree of methylation and the Ddah2 gene expression levels was found in both types of analyzed fragments. Total Hcy but not Hcy-S-proteins correlated with iNOS promoter methylation. Analyzed variants seem to contribute to the in vivo Hcy binding properties to IMA. The contribution of the Hcy-derived methylation modifications to Ddah2 and eNOS gene expression seems to be tissue-specific and independent of the Ddah2/ADMA/eNOS pathway. Hcy-derived methylation modifications to the iNOS gene promoter contribute to a lesser extent to iNOS gene expression.en_US
dc.languageengen_US
dc.relation.ispartofMolecular and Cellular Biochemistryen_US
dc.sourceMolecular And Cellular Biochemistry[ISSN 0300-8177],v. 369 (1-2), p. 235-246en_US
dc.subject32 Ciencias médicasen_US
dc.subject320102 Genética clínicaen_US
dc.subject.otherNitric-Oxide Synthaseen_US
dc.subject.otherMethylenetetrahydrofolate Reductaseen_US
dc.subject.otherAsymmetric Dimethylarginineen_US
dc.subject.otherRisk-Factoren_US
dc.subject.otherEndothelial-Cellsen_US
dc.subject.otherVascular-Diseaseen_US
dc.subject.otherDna Methylationen_US
dc.subject.otherGeneen_US
dc.subject.otherAtherosclerosisen_US
dc.subject.otherExpressionen_US
dc.titleHomocysteinylated protein levels in internal mammary artery (IMA) fragments and its genotype-dependence. S-Homocysteine-induced methylation modifications in IMA and aortic fragmentsen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1007/s11010-012-1387-7en_US
dc.identifier.scopus84865619653-
dc.identifier.isi000308067100025-
dcterms.isPartOfMolecular And Cellular Biochemistry-
dcterms.sourceMolecular And Cellular Biochemistry[ISSN 0300-8177],v. 369 (1-2), p. 235-246-
dc.contributor.authorscopusid6603262370-
dc.contributor.authorscopusid55308203100-
dc.contributor.authorscopusid55348741300-
dc.contributor.authorscopusid34970818700-
dc.contributor.authorscopusid8758145300-
dc.contributor.authorscopusid36099016000-
dc.contributor.authorscopusid7005446255-
dc.description.lastpage246en_US
dc.description.firstpage235en_US
dc.relation.volume369en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.identifier.wosWOS:000308067100025-
dc.contributor.daisngid1305938-
dc.contributor.daisngid17118663-
dc.contributor.daisngid13637672-
dc.contributor.daisngid9299806-
dc.contributor.daisngid5660229-
dc.contributor.daisngid1700450-
dc.contributor.daisngid245684-
dc.identifier.investigatorRIDD-2810-2013-
dc.identifier.investigatorRIDC-1247-2010-
dc.identifier.investigatorRIDNo ID-
dc.description.numberofpages12en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Rodriguez-Esparragon, F-
dc.contributor.wosstandardWOS:Serna-Gomez, JA-
dc.contributor.wosstandardWOS:Hernandez-Velazquez, E-
dc.contributor.wosstandardWOS:Buset-Rios, N-
dc.contributor.wosstandardWOS:Hernandez-Trujillo, Y-
dc.contributor.wosstandardWOS:Garcia-Bello, MA-
dc.contributor.wosstandardWOS:Rodriguez-Perez, JC-
dc.date.coverdateOctubre 2012en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.sjr0,948-
dc.description.jcr2,329-
dc.description.sjrqQ2-
dc.description.jcrqQ3-
dc.description.scieSCIE-
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptGIR IUIBS: Patología médica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Médicas y Quirúrgicas-
crisitem.author.orcid0000-0003-1663-3673-
crisitem.author.orcid0000-0003-0023-1063-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameRodríguez Esparragón, Francisco Javier-
crisitem.author.fullNameRodríguez Pérez, José Carlos-
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