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Endothelial ADAM17 expression in the progression of kidney injury in an obese mouse model of pre-diabetes

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dc.contributor.author Palau González, Vanesa
dc.contributor.author Jarrín, Josué
dc.contributor.author Villanueva, Sofia
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, 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 2022-09-23T06:23:36Z
dc.date.available 2022-09-23T06:23:36Z
dc.date.issued 2021
dc.identifier.citation Palau V, Jarrín J, Villanueva S, Benito D, Márquez E, Rodríguez E, Soler MJ, Oliveras A, Gimeno J, Sans L, Crespo M, Pascual J, Barrios C, Riera M. Endothelial ADAM17 expression in the progression of kidney injury in an obese mouse model of pre-diabetes. Int J Mol Sci. 2021 Dec 25;23(1):221. DOI: 10.3390/ijms23010221
dc.identifier.issn 1422-0067
dc.identifier.uri http://hdl.handle.net/10230/54170
dc.description.abstract Disintegrin and metalloproteinase domain 17 (ADAM17) activates inflammatory and fibrotic processes through the shedding of various molecules such as Tumor Necrosis Factor-α (TNF-α) or Transforming Growht Factor-α (TGF-α). There is a well-recognised link between TNF-α, obesity, inflammation, and diabetes. In physiological situations, ADAM17 is expressed mainly in the distal tubular cell while, in renal damage, its expression increases throughout the kidney including the endothelium. The aim of this study was to characterize, for the first time, an experimental mouse model fed a high-fat diet (HFD) with a specific deletion of Adam17 in endothelial cells and to analyse the effects on different renal structures. Endothelial Adam17 knockout male mice and their controls were fed a high-fat diet, to induce obesity, or standard rodent chow, for 22 weeks. Glucose tolerance, urinary albumin-to-creatinine ratio, renal histology, macrophage infiltration, and galectin-3 levels were evaluated. Results showed that obese mice presented higher blood glucose levels, dysregulated glucose homeostasis, and higher body weight compared to control mice. In addition, obese wild-type mice presented an increased albumin-to-creatinine ratio; greater glomerular size and mesangial matrix expansion; and tubular fibrosis with increased galectin-3 expression. Adam17 deletion decreased the albumin-to-creatinine ratio, glomerular mesangial index, and tubular galectin-3 expression. Moreover, macrophage infiltration in the glomeruli of obese Adam17 knockout mice was reduced as compared to obese wild-type mice. In conclusion, the expression of ADAM17 in endothelial cells impacted renal inflammation, modulating the renal function and histology in an obese pre-diabetic mouse model.
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher MDPI
dc.relation.ispartof Int J Mol Sci. 2021 Dec 25;23(1):221
dc.rights © 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 (https://creativecommons.org/licenses/by/4.0/).
dc.rights.uri https://creativecommons.org/licenses/by/4.0/
dc.title Endothelial ADAM17 expression in the progression of kidney injury in an obese mouse model of pre-diabetes
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.3390/ijms23010221
dc.subject.keyword ADAM17
dc.subject.keyword Endothelial cells
dc.subject.keyword Obesity
dc.subject.keyword Pre-diabetes
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion


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