The genetics of hypertension modifies the renal cell replication response induced by experimental diabetes

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dc.contributor.authorSilveira, L. A.
dc.contributor.authorBacchi, C. E.
dc.contributor.authorPinto, G. A.
dc.contributor.authorde Faria, JBL
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:36:59Z
dc.date.available2014-05-20T13:36:59Z
dc.date.issued2002-05-01
dc.description.abstractTo investigate whether the genetics of hypertension modifies renal cell responses in experimental diabetes, we studied the renal cell replication and its regulation by two cyclin-dependent kinase (Cdk) inhibitors, p27(Kip1) and p21(Cip1), in prehypertensive spontaneously hypertensive rats (SUR) and their genetically normotensive counterparts, Wistar Kyoto (WKY) rats, with and without streptozotocin-induced diabetes. In diabetic SIIR, the number of proliferating glomerular (0.6 +/- 0.3 positive cells/50 glomeruli) and tubulointerstitial (2.8 +/- 0.6 positive tubulointerstitial cells/50 grid fields) cells assessed by the bromodeoxyuridine technique was significantly (P = 0.0002) lower than in control SIIR (13.2 +/- 1.7 and 48.6 +/- 9.7, respectively) and control (14.0 +/- 1.8 and 63.9 +/- 10.6) and diabetic (14.3 +/- 3.5 and 66.4 +/- 11.5) WKY rats. Proliferating cell nuclear antigen, another marker of cell proliferation, was significantly reduced in replicating glomerular (P = 0.0002) and tubulointerstitial (P < 0.0001) cells in diabetic SHR. In freshly isolated glomeruli, the level of p27(Kip1) detected by Western blotting was significantly higher In diabetic SIIR than in nondiabetic SHR (1.52 +/- 0.14 vs. 1.00 +/- 0.10% of control, P = 0.014). The expression of p21(Cip1) in isolated glomeruli did not differ among the groups of rats. In conclusion, the response of renal cell replication to diabetes differs markedly between prehypertensive SIIR and their WKY control rats. The decreased glomerular cell proliferation in prehypertensive diabetic SIIR is at least partly mediated by a higher expression of the Cdk inhibitor p27(Kip1).en
dc.description.affiliationUNICAMP, Fac Med Sci, Nephrol Unit, Renal Pathophysiol Lab, Campinas, SP, Brazil
dc.description.affiliationUniv Estadual Paulista Julio Mesquita Filho, Fac Med Sci, Dept Pathol, Botucatu, SP, Brazil
dc.description.affiliationUNICAMP, Univ Hosp, Expt Pathol Lab, Campinas, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista Julio Mesquita Filho, Fac Med Sci, Dept Pathol, Botucatu, SP, Brazil
dc.format.extent1529-1534
dc.identifierhttp://dx.doi.org/10.2337/diabetes.51.5.1529
dc.identifier.citationDiabetes. Alexandria: Amer Diabetes Assoc, v. 51, n. 5, p. 1529-1534, 2002.
dc.identifier.doi10.2337/diabetes.51.5.1529
dc.identifier.issn0012-1797
dc.identifier.urihttp://hdl.handle.net/11449/12750
dc.identifier.wosWOS:000175492400028
dc.language.isoeng
dc.publisherAmer Diabetes Assoc
dc.relation.ispartofDiabetes
dc.relation.ispartofjcr7.273
dc.relation.ispartofsjr4,435
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.titleThe genetics of hypertension modifies the renal cell replication response induced by experimental diabetesen
dc.typeArtigo
dcterms.licensehttp://diabetes.diabetesjournals.org/site/misc/ifora.xhtml#Section4
dcterms.rightsHolderAmer Diabetes Assoc
unesp.author.orcid0000-0003-2373-5539[4]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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