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dc.contributor.CRUESPUniversidade Estadual de Campinaspt_BR
dc.typeArtigo de periódicopt_BR
dc.titleCharacterization of the insulin-signaling pathway in lacrimal and salivary glands of ratspt_BR
dc.contributor.authorRocha, EMpt_BR
dc.contributor.authorLima, MHDpt_BR
dc.contributor.authorCarvalho, CROpt_BR
dc.contributor.authorSaad, MJApt_BR
dc.contributor.authorVelloso, LApt_BR
unicamp.authorUniv Estadual Campinas, Sch Med, Fac Ciencias Med, Dept Clin Med,Lab Clin Physiopathol, BR-13081970 Campinas, SP, Brazilpt_BR
dc.subjectinsulin receptorpt_BR
dc.subjectIGF-1Rpt_BR
dc.subjectlacrimal glandpt_BR
dc.subjectsalivary glandpt_BR
dc.subjectsignal transductionpt_BR
dc.subject.wosFactor-i Receptorpt_BR
dc.subject.wosDiabetes-mellituspt_BR
dc.subject.wosGrowth-factorspt_BR
dc.subject.wosPhosphatidylinositol 3-kinasept_BR
dc.subject.wosTyrosine Phosphorylationpt_BR
dc.subject.wosTransduction Pathwayspt_BR
dc.subject.wosSteroid-hormonespt_BR
dc.subject.wosAnimal-modelspt_BR
dc.subject.wosMusclept_BR
dc.subject.wosLiverpt_BR
dc.description.abstractPurpose. Insulin has been acknowledged as a mediator of several physiological events in lacrimal and salivary glands. We investigated the presence of insulin receptors and of insulin-induced autophosphorylation of the insulin receptor and activation of elements involved in the early steps of insulin signaling in lacrimal and salivary glands of rats. Methods. Lacrimal and salivary glands of Wistar rats were removed and processed for immunohistochemistry using antiinsulin receptor and anti-IGF-1 receptor antibodies. The activation of insulin receptors following insulin treatment, and the involvement of insulin receptor substrates-1 and -2, Shc, JAK-2 and STAT-1, were analyzed by immunoprecipitation, followed by SDS-PAGE and immunoblotting of rat lacrimal and salivary glands after exposure to insulin. Results. Insulin and IGF-1 receptors were present in rat lacrimal and salivary glands and were located predominantly in the cytoplasm and plasma membrane. Functional studies demonstrated that insulin induced a dose-dependent phosphorylation of the insulin receptor, IGF-1R, insulin receptor substrates-1 and -2, Shc, and STAT-1. In rats with streptozotocin-induced diabetes mellitus there was a significant reduction in insulin-induced insulin receptor and STAT-1 phosphorylation in the lacrimal gland but not in the salivary gland; there was no influence on Shc phosphorylation in either tissue. Conclusions. The present results indicate that insulin and IGF-1 receptors are expressed in lacrimal and salivary glands, and that insulin can induce the phosphorylation of its receptor and activate elements involved in the early steps of insulin signaling in both tissues.pt
dc.relation.ispartofCurrent Eye Researchpt_BR
dc.relation.ispartofabbreviationCurr. Eye Res.pt_BR
dc.publisher.cityLissept_BR
dc.publisher.countryHolandapt_BR
dc.publisherSwets Zeitlinger Publisherspt_BR
dc.date.issued2000pt_BR
dc.identifier.citationCurrent Eye Research. Swets Zeitlinger Publishers, v. 21, n. 5, n. 833, n. 842, 2000.pt_BR
dc.language.isoenpt_BR
dc.description.volume21pt_BR
dc.description.issuenumber5pt_BR
dc.description.firstpage833pt_BR
dc.description.lastpage842pt_BR
dc.rightsfechadopt_BR
dc.sourceWeb of Sciencept_BR
dc.identifier.issn0271-3683pt_BR
dc.identifier.wosidWOS:000166735700001pt_BR
dc.identifier.doi10.1076/ceyr.21.5.833.5535pt_BR
dc.date.available2014-12-02T16:30:17Z
dc.date.available2015-11-26T17:39:35Z-
dc.date.accessioned2014-12-02T16:30:17Z
dc.date.accessioned2015-11-26T17:39:35Z-
dc.description.provenanceMade available in DSpace on 2014-12-02T16:30:17Z (GMT). No. of bitstreams: 1 WOS000166735700001.pdf: 329047 bytes, checksum: 5982c1657511416af34c0aa40925b309 (MD5) Previous issue date: 2000en
dc.description.provenanceMade available in DSpace on 2015-11-26T17:39:35Z (GMT). No. of bitstreams: 2 WOS000166735700001.pdf: 329047 bytes, checksum: 5982c1657511416af34c0aa40925b309 (MD5) WOS000166735700001.pdf.txt: 39701 bytes, checksum: 5b991178ac0d941d47674d8c0d1934ef (MD5) Previous issue date: 2000en
dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/62907pt_BR
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/62907
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/62907-
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