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Redefining the role of ADAM17 in renal proximal tubular cells and its implications in an obese mouse model of pre-diabetes

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dc.contributor.author Palau González, Vanesa
dc.contributor.author Villanueva, Sofia
dc.contributor.author Jarrín, Josué
dc.contributor.author Benito, David
dc.contributor.author Márquez, Eva
dc.contributor.author Rodríguez, Eva
dc.contributor.author Soler, María José
dc.contributor.author Oliveras, Anna
dc.contributor.author Gimeno Beltran, Javier
dc.contributor.author Sans Atxer, Laia
dc.contributor.author Crespo Barrio, Marta
dc.contributor.author Pascual Santos, Julio
dc.contributor.author Barrios Barrera, Clara
dc.contributor.author Riera Oliva, Marta
dc.date.accessioned 2022-09-05T06:38:50Z
dc.date.available 2022-09-05T06:38:50Z
dc.date.issued 2021
dc.identifier.citation Palau V, Villanueva S, Jarrín J, Benito D, Márquez E, Rodríguez E, et al. Redefining the role of ADAM17 in renal proximal tubular cells and its implications in an obese mouse model of pre-diabetes. Int J Mol Sci. 2021 Dec 3; 22(23): 13093. DOI: 10.3390/ijms222313093
dc.identifier.issn 1422-0067
dc.identifier.uri http://hdl.handle.net/10230/53991
dc.description.abstract Acute and chronic kidney lesions induce an increase in A Disintegrin And Metalloproteinase domain 17 (ADAM17) that cleaves several transmembrane proteins related to inflammatory and fibrotic pathways. Our group has demonstrated that renal ADAM17 is upregulated in diabetic mice and its inhibition decreases renal inflammation and fibrosis. The purpose of the present study was to analyze how Adam17 deletion in proximal tubules affects different renal structures in an obese mice model. Tubular Adam17 knockout male mice and their controls were fed a high-fat diet (HFD) for 22 weeks. Glucose tolerance, urinary albumin-to-creatinine ratio, renal histology, and pro-inflammatory and pro-fibrotic markers were evaluated. Results showed that wild-type mice fed an HFD became obese with glucose intolerance and renal histological alterations mimicking a pre-diabetic condition; consequently, greater glomerular size and mesangial expansion were observed. Adam17 tubular deletion improved glucose tolerance and protected animals against glomerular injury and prevented podocyte loss in HFD mice. In addition, HFD mice showed more glomerular macrophages and collagen accumulation, which was prevented by Adam17 deletion. Galectin-3 expression increased in the proximal tubules and glomeruli of HFD mice and ameliorated with Adam17 deletion. In conclusion, Adam17 in proximal tubules influences glucose tolerance and participates in the kidney injury in an obese pre-diabetic murine model. The role of ADAM17 in the tubule impacts on glomerular inflammation and fibrosis.
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher MDPI
dc.rights Copyright © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
dc.rights.uri http://creativecommons.org/licenses/by/4.0/
dc.title Redefining the role of ADAM17 in renal proximal tubular cells and its implications in an obese mouse model of pre-diabetes
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.3390/ijms222313093
dc.subject.keyword ADAM17
dc.subject.keyword Obesity
dc.subject.keyword Pre-diabetes
dc.subject.keyword Renal proximal tubular cells
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion


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