Effects of sunitinib on immunoreactivity of vimentin, E-cadherin and S100 in kidneys of streptozotocin induced diabetic mice

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dc.contributor.authorAkarca-Dizakar, S. O.
dc.contributor.authorAktug, H.
dc.contributor.authorOltulu, F.
dc.contributor.authorOktem, G.
dc.contributor.authorYavasoglu, A.
dc.contributor.authorAcikgoz, E.
dc.contributor.authorYigitturk, G.
dc.contributor.authorDemir, K.
dc.contributor.authorUysal, A.
dc.date.accessioned2019-10-27T10:45:02Z
dc.date.available2019-10-27T10:45:02Z
dc.date.issued2018
dc.departmentEge Üniversitesien_US
dc.description.abstractDiabetes mellitus (DM) affects many organs including kidney. Tyrosine kinase can cause hypoglycemia and sunitinib is an inhibitor of tyrosine kinase. We investigated the possible effects of sunitinib on the kidney of streptozotocin (STZ) induced type 1 diabetic mice. We used 28 CD 1 type male mice divided into four groups of seven. Type 1 diabetes was induced by injection of STZ. Group 1 was the untreated control. Group 2 comprised non-diabetic mice + sunitinib. Both groups 1 and 2 exhibited normal blood glucose levels. Group 3 comprised STZ treated diabetic mice + saline. Group 4 were diabetic mice + sunitinib treatment. Kidneys were removed after 8weeks. The immunoreactivities of vimentin, E-cadherin and S100 were assessed. Immunostaining of vimentin, E-cadherin and S100 was located in both the glomeruli and tubules of the kidney. We found that the number of vimentin and E-cadherin positive glomeruli and tubules were increased after sunitinib treatment compared to saline treated diabetic mice. The number of vimentin labeled tubules was decreased in the sunitinib treated group compared to diabetic + saline groups. Differences in the number of S100 positive tubules and glomeruli between groups 3 and 4 were not statistically significant. The effect of sunitinib on experimental diabetic mice appears to be related to levels of vimentin, E-cadherin and S100 in the glomeruli and tubules of the kidney, and sunitinib may protect against renal damage from DM.en_US
dc.identifier.doi10.1080/10520295.2018.1439532en_US
dc.identifier.endpage335en_US
dc.identifier.issn1052-0295
dc.identifier.issn1473-7760
dc.identifier.issue5en_US
dc.identifier.pmid29652183en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage328en_US
dc.identifier.urihttps://doi.org/10.1080/10520295.2018.1439532
dc.identifier.urihttps://hdl.handle.net/11454/31078
dc.identifier.volume93en_US
dc.identifier.wosWOS:000447175700003en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofBiotechnic & Histochemistryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectDiabetes mellitusen_US
dc.subjecte-cadherinen_US
dc.subjectkidneyen_US
dc.subjectmiceen_US
dc.subjectS100en_US
dc.subjectstreptozotocinen_US
dc.subjectsunitiniben_US
dc.subjecttyrosine kinase inhibitoren_US
dc.subjectvimentinen_US
dc.titleEffects of sunitinib on immunoreactivity of vimentin, E-cadherin and S100 in kidneys of streptozotocin induced diabetic miceen_US
dc.typeArticleen_US

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