Calcium oxalate crystals and oxalate induce an epithelial-to-mesenchymal transition in the proximal tubular epithelial cells: Contribution to oxalate kidney injury

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dc.citation.volume7
dc.contributor.authorConvento, Marcia Bastos [UNIFESP]
dc.contributor.authorPessoa, Edson Andrade [UNIFESP]
dc.contributor.authorCruz, Edgar [UNIFESP]
dc.contributor.authorda Gloria, Maria Aparecida [UNIFESP]
dc.contributor.authorSchor, Nestor [UNIFESP]
dc.contributor.authorBorges, Fernanda Teixeira [UNIFESP]
dc.coverageLondon
dc.date.accessioned2020-07-17T14:02:17Z
dc.date.available2020-07-17T14:02:17Z
dc.date.issued2017
dc.description.abstractTGF-beta 1 is the main mediator of epithelial-to-mesenchymal transition (EMT). Hyperoxaluria induces crystalluria, interstitial fibrosis, and progressive renal failure. This study analyzed whether hyperoxaluria is associated with TGF-beta 1 production and kidney fibrosis in mice and if oxalate or calcium oxalate (CaOx) could induce EMT in proximal tubule cells (HK2) and therefore contribute to the fibrotic process. Hyperoxaluria was induced by adding hydroxyproline and ethylene glycol to the mice's drinking water for up to 60 days. Renal function and oxalate and urinary crystals were evaluated. Kidney collagen production and TGF-beta 1 expression were assessed. EMT was analyzed in vitro according to TGF-beta 1 production, phenotypic characterization, invasion, cell migration, gene and protein expression of epithelial and mesenchymal markers. Hyperoxaluric mice showed a decrease in renal function and an increase in CaOx crystals and Ox urinary excretion. The deposition of collagen in the renal interstitium was observed. HK2 cells stimulated with Ox and CaOx exhibited a decreased expression of epithelial as well as increased expression mesenchymal markersen
dc.description.abstractthese cells presented mesenchymal phenotypic changes, migration, invasiveness capability and TGF-beta 1 production, characterizing EMT. Treatment with BMP-7 or its overexpression in HK2 cells was effective at preventing it. This mechanism may contribute to the fibrosis observed in hyperoxaluria.en
dc.description.affiliationUniv Fed Sao Paulo UNIFESP, Nephrol Div, Dept Med, Sao Paulo, SP, Brazil
dc.description.affiliationUniv Cruzeiro Sul, CBS, Hlth Sci, Postgrad Program, Sao Paulo, Brazil
dc.description.affiliationCNPq Conselho Nacl Desenvolvimento Cient & Tecnol, Brasilia, DF, Brazil
dc.description.affiliationCAPES Coordenacao Aperfeicoamento Pessoal Nivel S, Brasilia, DF, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo UNIFESP, Nephrol Div, Dept Med, Sao Paulo, SP, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo)
dc.description.sponsorshipCNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico)
dc.description.sponsorshipCAPES (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior)
dc.format.extent-
dc.identifierhttp://dx.doi.org/10.1038/srep45740
dc.identifier.citationScientific Reports. London, v. 7, p. -, 2017.
dc.identifier.doi10.1038/srep45740
dc.identifier.fileWOS000398554800001.pdf
dc.identifier.issn2045-2322
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/54723
dc.identifier.wosWOS:000398554800001
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofScientific Reports
dc.rightsinfo:eu-repo/semantics/openAccess
dc.titleCalcium oxalate crystals and oxalate induce an epithelial-to-mesenchymal transition in the proximal tubular epithelial cells: Contribution to oxalate kidney injuryen
dc.typeinfo:eu-repo/semantics/article
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