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dc.contributor.authorSgarbosa, Fabio [UNESP]
dc.contributor.authorBarbisan, Luis Fernando [UNESP]
dc.contributor.authorBrasil, Maria A. M. [UNESP]
dc.contributor.authorCosta, Elaine [UNESP]
dc.contributor.authorCalderon, Iracema de Mattos Paranhos [UNESP]
dc.contributor.authorGoncalves, Claudia R.
dc.contributor.authorBevilacqua, Estela [UNESP]
dc.contributor.authorRudge, Marilza Vieira Cunha [UNESP]
dc.date.accessioned2014-05-20T13:35:05Z
dc.date.available2014-05-20T13:35:05Z
dc.date.issued2006-08-01
dc.identifierhttp://dx.doi.org/10.1016/j.diabres.2005.12.014
dc.identifier.citationDiabetes Research and Clinical Practice. Clare: Elsevier B.V., v. 73, n. 2, p. 143-149, 2006.
dc.identifier.issn0168-8227
dc.identifier.urihttp://hdl.handle.net/11449/12039
dc.description.abstractApoptosis and its associated regulatory mechanisms are physiological events crucial to the maintenance of placental homeostasis; imbalance of these processes, however, such as occurs under various pathological conditions, may compromise placenta function and, consequently, pregnancy success. Increased apoptosis occurs in the placentas of pregnant women with several developmental disabilities, while increased Bcl-2 expression is generally associated with pregnancy-associated tumors. Herein, we tested the hypothesis that apoptosis-associated disturbs might be involved in the placental physiopathology subjected to different maternal hyperglycemic conditions.Thus, in the present study we investigated and compared the incidence of apoptosis using TUNEL reaction and Bcl-2 expression, in term-placentas of normoglycemic, diabetic and daily hyperglycemic patients. Tissue samples were collected from 37 placentas, being 15 from healthy mothers with normally delivered healthy babies, and 22 from mothers with glucose disturbances. From these latter 22 patients, 10 showed maternal daily hyperglycemia and 12 were clinically diabetics. Both Bcl-2 expression and apoptotic DNA fragmentation were established and quantified in the trophoblasts of healthy mothers. Compared to these reference values, a higher apoptosis index and lower Bcl-2 expression were disclosed in the placentas of the diabetic women, while in the daily hyperglycemic group, values were intermediate between the diabetic and normoglycemic patients. The TUNEL/Bcl-2 index ratio in the placentas varied from 0.02 to 0.09 for pregnant normoglycemic and diabetic women, respectively, revealing a predominance of apoptosis in the diabetic group. Our findings suggest that hyperglycemia may be a key factor evoking apoptosis in the placental trophoblast, and therefore, is relevant to diabetic placenta function. (c) 2006 Elsevier B.V.. All rights reserved.en
dc.format.extent143-149
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofDiabetes Research and Clinical Practice
dc.sourceWeb of Science
dc.subjectdiabetespt
dc.subjectcell deathpt
dc.subjectproliferationpt
dc.subjectsyncytiotrophoblastpt
dc.subjectTUNEL reactionpt
dc.titleChanges in apoptosis and Bcl-2 expression in human hyperglycemic, term placental trophoblasten
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.description.affiliationUniv Estadual Paulista Julio Mesquita Filho, Sch Med, Dept Gynecol & Obstet, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUniv São Paulo, Inst Biomed Sci, Dept Cellular & Dev Biol, BR-05508900 São Paulo, Brazil
dc.description.affiliationUnespUniv Estadual Paulista Julio Mesquita Filho, Sch Med, Dept Gynecol & Obstet, BR-18618000 Botucatu, SP, Brazil
dc.identifier.doi10.1016/j.diabres.2005.12.014
dc.identifier.wosWOS:000239285800004
dc.rights.accessRightsAcesso restrito
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt
dc.identifier.lattes0679387622604743
dc.identifier.lattes6758680388835078
dc.identifier.orcid0000-0002-9227-832X
unesp.author.lattes0679387622604743
unesp.author.lattes6758680388835078
unesp.author.orcid0000-0002-9227-832X[8]
unesp.author.orcid0000-0003-4178-4625[7]
unesp.author.orcid0000-0003-4761-4336[5]
dc.relation.ispartofjcr2.548
dc.relation.ispartofsjr1,538
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