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Oestrogen supplementation following castration promotes stromal remodelling and histopathological alterations in the Mongolian gerbil ventral prostate

dc.contributor.authorScarano, Wellerson Rodrigo
dc.contributor.authorde Sousa, Daniel Emidio [UNESP]
dc.contributor.authorCampos, Silvana Gisele Pegorin [UNESP]
dc.contributor.authorCorradi, Lara Silvia
dc.contributor.authorVilamaior, Patricia Simone Leite
dc.contributor.authorTaboga, Sebastiao Roberto [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionRio Preto Univ Ctr UNIRP
dc.date.accessioned2014-05-20T14:00:59Z
dc.date.available2014-05-20T14:00:59Z
dc.date.issued2008-02-01
dc.description.abstractThe effect of oestradiol on the intact and castrated adult gerbil prostate was evaluated by focussing on stromal and epithelial disorders, and hormonal receptor immunoreactivity. The experimental animals were studied by histological, histochemical and immunohistochemical techniques, morphometric-stereological analysis and transmission electron microscopy. Epithelial alterations in the oestradiol-treated animals were frequent, with an increase in epithelial cell height, areas of intense dysplasia and hyperplasia and formation of prostatic intraepithelial neoplasia (PIN). Another aspect that did not depend on the presence of testosterone was the arrangement of the fibrillar and non-fibrillar elements of the extracellular matrix among smooth muscle cells (SMC), suggesting a possible role of these cells in rearrangement and synthesis of these components, after oestrogenic treatment. In the castrated animals, an accumulation of extracellular matrix elements under the epithelium was evident, while in the intact animals the same compounds were dispersed and scarce. In the groups of intact and castrated animals, SMC and fibroblasts exhibited a secretory phenotype, which was accentuated after oestradiol administration. There was an increase of the immunoreactivity to alpha-oestrogen and androgen receptors in hyperplastic areas compared to normal epithelium, revealing the involvement of these steroid receptors in the hyperplasia and PIN development.en
dc.description.affiliationSão Paulo State Univ IBILCE UNESP, Dept Biol, Microscopy & Microanal Lab, BR-15054000 Sao Jose do Rio Preto, SP, Brazil
dc.description.affiliationUniv Estadual Campinas, Inst Biol, Dept Cell Biol, Campinas, SP, Brazil
dc.description.affiliationRio Preto Univ Ctr UNIRP, Sch Biol Sci, Sao Jose do Rio Preto, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ IBILCE UNESP, Dept Biol, Microscopy & Microanal Lab, BR-15054000 Sao Jose do Rio Preto, SP, Brazil
dc.format.extent25-37
dc.identifierhttp://dx.doi.org/10.1111/j.1365-2613.2007.00559.x
dc.identifier.citationInternational Journal of Experimental Pathology. Oxford: Blackwell Publishing, v. 89, n. 1, p. 25-37, 2008.
dc.identifier.doi10.1111/j.1365-2613.2007.00559.x
dc.identifier.issn0959-9673
dc.identifier.lattes3713732996827351
dc.identifier.lattes7066358123790434
dc.identifier.orcid0000-0002-0970-4288
dc.identifier.orcid0000-0001-9559-5497
dc.identifier.urihttp://hdl.handle.net/11449/21543
dc.identifier.wosWOS:000252261100003
dc.language.isoeng
dc.publisherBlackwell Publishing
dc.relation.ispartofInternational Journal of Experimental Pathology
dc.relation.ispartofjcr1.938
dc.relation.ispartofsjr0,712
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectcastrationen
dc.subjectepitheliumen
dc.subjectgerbilen
dc.subjectoestradiolen
dc.subjectprostateen
dc.subjectstromaen
dc.titleOestrogen supplementation following castration promotes stromal remodelling and histopathological alterations in the Mongolian gerbil ventral prostateen
dc.typeArtigo
dcterms.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dcterms.rightsHolderBlackwell Publishing
dspace.entity.typePublication
unesp.author.lattes3713732996827351
unesp.author.lattes7066358123790434[5]
unesp.author.orcid0000-0001-9559-5497[5]
unesp.author.orcid0000-0002-6682-2934[1]
unesp.author.orcid0000-0002-0970-4288[6]

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