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Endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice
BACKGROUND: Hypercholesterolemia is a well-established risk factor for the development of kidney injury. Considering that female sex hormones may play a preventative role in both cardiovascular and renal diseases, the aim of the present study was to evaluate the effects of female sex hormones on hyp...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4280709/ https://www.ncbi.nlm.nih.gov/pubmed/25422135 http://dx.doi.org/10.1186/1476-511X-13-176 |
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author | Carneiro, Sonila S Carminati, Raffaela Z Freitas, Flavia PS Podratz, Priscila L Balarini, Camille M Graceli, Jones B Meyrelles, Silvana S Vasquez, Elisardo C Gava, Agata L |
author_facet | Carneiro, Sonila S Carminati, Raffaela Z Freitas, Flavia PS Podratz, Priscila L Balarini, Camille M Graceli, Jones B Meyrelles, Silvana S Vasquez, Elisardo C Gava, Agata L |
author_sort | Carneiro, Sonila S |
collection | PubMed |
description | BACKGROUND: Hypercholesterolemia is a well-established risk factor for the development of kidney injury. Considering that female sex hormones may play a preventative role in both cardiovascular and renal diseases, the aim of the present study was to evaluate the effects of female sex hormones on hypercholesterolemia-induced renal dysfunction. METHODS: Apolipoprotein E-deficient (ApoE) and C57 control female mice underwent an ovariectomy (OVX) or sham surgery and after 2 months, creatinine clearance, uremia and proteinuria were determined. Renal oxidative stress and lipid deposition were also quantified. Values are presented as mean ± SEM. Statistical analyses were performed using Two-way ANOVA followed by Tukey’s post hoc test. RESULTS: Creatinine clearance (μL/min) was similar between C57 (171 ± 17) and ApoE (140 ± 26) mice underwent sham surgery. OVX resulted in a reduced glomerular filtration rate in both C57 (112 ± 8, ~ − 35%, p < 0.05) and ApoE (61 ± 10, ~ − 56%, p < 0.05) animals. Plasma levels of urea (mg/dL) were higher in both ApoE groups (Sham: 73 ± 7; OVX: 73 ± 8, p < 0.05) when compared to C57 animals (Sham: 49 ± 3; OVX: 60 ± 4), with no changes among ovariectomized groups. Proteinuria levels (mg/24 h) were similar between C57 (Sham: 25.1 ± 5.7; OVX: 33.7 ± 4.7) and ApoE sham animals (26.4 ± 3.5), however, 24-h urine protein excretion was augmented in ApoE OVX animals (49.6 ± 5.8, p < 0.05). Histological kidney analysis demonstrated that the absence of female sex hormones resulted in increased oxidative stress, which was more severe in ApoE mice (C57 Sham: 9.2 ± 0.4; C57 OVX: 22.9 ± 1.0; ApoE Sham: 13.9 ± 0.7; ApoE OVX: 34.0 ± 1.4 au x 10(3), p < 0.05). As expected, ApoE mice presented higher lipid deposition, which was not affected by OVX (C57 Sham: 0 ± 0; C57 OVX: 0 ± 0; ApoE Sham: 6.8 ± 1.6; ApoE OVX: 5.2 ± 0.8% x 10(−2), p < 0.05). Ovariectomy resulted in a similar reduction in ER-α protein expression in the renal cortex (C57: 0.78 ± 0.04; ApoE: 0.81 ± 0.04 au, p < 0.05) when compared to sham animals (C57:1.00 ± 0.04; ApoE: 1.03 ± 0.03 au). CONCLUSION: Taken together these data indicate that female sex hormones may delay hypercholesterolemia-induced renal dysfunction and emphasizes the importance of plasma cholesterol control in post-menopausal women. |
format | Online Article Text |
id | pubmed-4280709 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-42807092015-01-01 Endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice Carneiro, Sonila S Carminati, Raffaela Z Freitas, Flavia PS Podratz, Priscila L Balarini, Camille M Graceli, Jones B Meyrelles, Silvana S Vasquez, Elisardo C Gava, Agata L Lipids Health Dis Research BACKGROUND: Hypercholesterolemia is a well-established risk factor for the development of kidney injury. Considering that female sex hormones may play a preventative role in both cardiovascular and renal diseases, the aim of the present study was to evaluate the effects of female sex hormones on hypercholesterolemia-induced renal dysfunction. METHODS: Apolipoprotein E-deficient (ApoE) and C57 control female mice underwent an ovariectomy (OVX) or sham surgery and after 2 months, creatinine clearance, uremia and proteinuria were determined. Renal oxidative stress and lipid deposition were also quantified. Values are presented as mean ± SEM. Statistical analyses were performed using Two-way ANOVA followed by Tukey’s post hoc test. RESULTS: Creatinine clearance (μL/min) was similar between C57 (171 ± 17) and ApoE (140 ± 26) mice underwent sham surgery. OVX resulted in a reduced glomerular filtration rate in both C57 (112 ± 8, ~ − 35%, p < 0.05) and ApoE (61 ± 10, ~ − 56%, p < 0.05) animals. Plasma levels of urea (mg/dL) were higher in both ApoE groups (Sham: 73 ± 7; OVX: 73 ± 8, p < 0.05) when compared to C57 animals (Sham: 49 ± 3; OVX: 60 ± 4), with no changes among ovariectomized groups. Proteinuria levels (mg/24 h) were similar between C57 (Sham: 25.1 ± 5.7; OVX: 33.7 ± 4.7) and ApoE sham animals (26.4 ± 3.5), however, 24-h urine protein excretion was augmented in ApoE OVX animals (49.6 ± 5.8, p < 0.05). Histological kidney analysis demonstrated that the absence of female sex hormones resulted in increased oxidative stress, which was more severe in ApoE mice (C57 Sham: 9.2 ± 0.4; C57 OVX: 22.9 ± 1.0; ApoE Sham: 13.9 ± 0.7; ApoE OVX: 34.0 ± 1.4 au x 10(3), p < 0.05). As expected, ApoE mice presented higher lipid deposition, which was not affected by OVX (C57 Sham: 0 ± 0; C57 OVX: 0 ± 0; ApoE Sham: 6.8 ± 1.6; ApoE OVX: 5.2 ± 0.8% x 10(−2), p < 0.05). Ovariectomy resulted in a similar reduction in ER-α protein expression in the renal cortex (C57: 0.78 ± 0.04; ApoE: 0.81 ± 0.04 au, p < 0.05) when compared to sham animals (C57:1.00 ± 0.04; ApoE: 1.03 ± 0.03 au). CONCLUSION: Taken together these data indicate that female sex hormones may delay hypercholesterolemia-induced renal dysfunction and emphasizes the importance of plasma cholesterol control in post-menopausal women. BioMed Central 2014-11-25 /pmc/articles/PMC4280709/ /pubmed/25422135 http://dx.doi.org/10.1186/1476-511X-13-176 Text en © Carneiro et al.; licensee BioMed Central Ltd. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Carneiro, Sonila S Carminati, Raffaela Z Freitas, Flavia PS Podratz, Priscila L Balarini, Camille M Graceli, Jones B Meyrelles, Silvana S Vasquez, Elisardo C Gava, Agata L Endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice |
title | Endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice |
title_full | Endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice |
title_fullStr | Endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice |
title_full_unstemmed | Endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice |
title_short | Endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice |
title_sort | endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein e-deficient mice |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4280709/ https://www.ncbi.nlm.nih.gov/pubmed/25422135 http://dx.doi.org/10.1186/1476-511X-13-176 |
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