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dc.contributor.CRUESPUNIVERSIDADE DE ESTADUAL DE CAMPINASpt_BR
dc.typeArtigo de Periódicopt_BR
dc.titleProlactin, Egfr, Vimentin And Alpha-actin Profiles In Elderly Rat Prostate Subjected To Steroid Hormonal Imbalancept_BR
dc.contributor.authorHetzlpt_BR
dc.contributor.authorAC; Monticopt_BR
dc.contributor.authorF; Kidopt_BR
dc.contributor.authorLA; Cagnonpt_BR
dc.contributor.authorVHApt_BR
unicamp.author.emailquitete@unicamp.brpt_BR
dc.subjectProstatept_BR
dc.subjectRatpt_BR
dc.subjectProlactinpt_BR
dc.subjectEgfrpt_BR
dc.subjectVimentin And Alpha-actinpt_BR
dc.description.abstractThe aim of this study was to characterize and relate the prolactin (PR), epidermal growth factor receptor (EGFR), alpha-actin and vimentin immunoreactivity in the prostate of elderly rats subjected to steroid hormonal imbalance. Senile and young rats were divided into the young group (YNG), the senile group (SE), the castrated group (CAS), the estrogen-deficient group (ED), the castrated + estrogen group (CASE), and the estrogen-deficient + androgen group (EDTEST). PR and EGFR increased in the estrogen and androgen ablation groups. In addition, EGFR influenced the immunolocalization by changing it from the prostatic stroma to the epithelium in elderly rats. Hormone ablation in elderly rats, not only related to androgen but also estrogen, led to increased stromal EGFR immunolocalization. The alpha-actin pattern decreased in the groups with estrogenic imbalance. Moreover, vimentin increased in the senile and estrogen deficient group. To conclude, we can suggest that EGFR contributed towards the proliferative process in the prostate, by means however, of different mechanisms, considering the androgenic and estrogenic pathways. Also, our results indicated that prolactin could be activated not only in an androgen-independent pathway but also in an estrogen independent pathway. Finally, PR and vimentin immunolocalization increase, in the prostatic stroma in the group showing estrogenic ablation, could be one of the factors which contribute to the reactive stroma formation. (C) 2016 Elsevier Ltd. All rights reserved.en
dc.relation.ispartofTissue & Cellpt_BR
dc.publisher.cityEDINBURGHpt_BR
dc.publisherCHURCHILL LIVINGSTONEpt_BR
dc.date.issued2016pt_BR
dc.identifier.citationTissue & Cell. CHURCHILL LIVINGSTONE, n. 48, n. 3, p. 189 - 196.pt_BR
dc.language.isoEnglishpt_BR
dc.description.volume48pt_BR
dc.description.issuenumberpt_BR
dc.description.firstpage189pt_BR
dc.description.lastpage196pt_BR
dc.rightsfechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn1532-3072pt_BR
dc.identifier.wosidWOS:000376396200006pt_BR
dc.identifier.doi10.1016/j.tice.2016.03.008pt_BR
dc.identifier.urlhttp://www-sciencedirect-com.ez88.periodicos.capes.gov.br/science/article/pii/S0040816615300124pt_BR
dc.description.sponsorshipSao Paulo Research Foundation (FAPESP) [2010/01739-1, 2009/50396-2]pt_BR
dc.description.sponsorship1Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.date.available2016-12-06T18:29:35Z-
dc.date.accessioned2016-12-06T18:29:35Z-
dc.description.provenanceMade available in DSpace on 2016-12-06T18:29:35Z (GMT). No. of bitstreams: 1 000376396200006.pdf: 2797864 bytes, checksum: 53cc4ab194aa49906d1af85e6fd4e8fb (MD5) Previous issue date: 2016en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/319811-
dc.description.conferencelocationpt_BR
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