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Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats

BACKGROUND: Chronic alcohol ingestion-induced kidney structure and function alterations are very well known, but the precise underlying molecular mediators involved in ethanol-induced kidney abnormalities remain elusive. The aim of this study was to investigate the effect of chronic ethanol exposure...

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Autores principales: Samadi, Mahrokh, Shirpoor, Alireza, Afshari, Ali Taghizadeh, Kheradmand, Fatemeh, Rasmi, Yousef, Sadeghzadeh, Maryam
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Akadémiai Kiadó 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6343583/
https://www.ncbi.nlm.nih.gov/pubmed/30713757
http://dx.doi.org/10.1556/1646.10.2018.23
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author Samadi, Mahrokh
Shirpoor, Alireza
Afshari, Ali Taghizadeh
Kheradmand, Fatemeh
Rasmi, Yousef
Sadeghzadeh, Maryam
author_facet Samadi, Mahrokh
Shirpoor, Alireza
Afshari, Ali Taghizadeh
Kheradmand, Fatemeh
Rasmi, Yousef
Sadeghzadeh, Maryam
author_sort Samadi, Mahrokh
collection PubMed
description BACKGROUND: Chronic alcohol ingestion-induced kidney structure and function alterations are very well known, but the precise underlying molecular mediators involved in ethanol-induced kidney abnormalities remain elusive. The aim of this study was to investigate the effect of chronic ethanol exposure on matrix metalloproteinase 2, 9 (MMP), glomerular filtration barrier proteins (nephrin and podocin), as well as vascular endothelial growth factor receptor 1, 2 (VEGFRs) isoforms gene expression in the kidney of rats. METHODS: Sixteen male Wistar rats with an initial body weight of 220 ± 10 g were divided into the following two groups: (1) control and (2) ethanol (4.5 g/kg BW). RESULTS: After 6 weeks of treatment, the results revealed a significant increase in isoforms VEGFR1 and VEGFR2 of VEGFR gene expression, significant increases of MMP2 and MMP9 activities, as well as significant decrease of nephrin and podocin gene expressions in the ethanol group, compared with that in the control group. CONCLUSION: These findings indicate that ethanol-induced kidney abnormalities may be in part associated with alteration in expressions of VEGFRs, nephrin, and podocin and in increasing activities of MMP2 and MMP9 as key molecular mediators in the kidney function.
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spelling pubmed-63435832019-02-01 Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats Samadi, Mahrokh Shirpoor, Alireza Afshari, Ali Taghizadeh Kheradmand, Fatemeh Rasmi, Yousef Sadeghzadeh, Maryam Interv Med Appl Sci Original Paper BACKGROUND: Chronic alcohol ingestion-induced kidney structure and function alterations are very well known, but the precise underlying molecular mediators involved in ethanol-induced kidney abnormalities remain elusive. The aim of this study was to investigate the effect of chronic ethanol exposure on matrix metalloproteinase 2, 9 (MMP), glomerular filtration barrier proteins (nephrin and podocin), as well as vascular endothelial growth factor receptor 1, 2 (VEGFRs) isoforms gene expression in the kidney of rats. METHODS: Sixteen male Wistar rats with an initial body weight of 220 ± 10 g were divided into the following two groups: (1) control and (2) ethanol (4.5 g/kg BW). RESULTS: After 6 weeks of treatment, the results revealed a significant increase in isoforms VEGFR1 and VEGFR2 of VEGFR gene expression, significant increases of MMP2 and MMP9 activities, as well as significant decrease of nephrin and podocin gene expressions in the ethanol group, compared with that in the control group. CONCLUSION: These findings indicate that ethanol-induced kidney abnormalities may be in part associated with alteration in expressions of VEGFRs, nephrin, and podocin and in increasing activities of MMP2 and MMP9 as key molecular mediators in the kidney function. Akadémiai Kiadó 2018-06-26 2018-09 /pmc/articles/PMC6343583/ /pubmed/30713757 http://dx.doi.org/10.1556/1646.10.2018.23 Text en © 2018 The Author(s) http://creativecommons.org/licenses/by-nc/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes – if any – are indicated.
spellingShingle Original Paper
Samadi, Mahrokh
Shirpoor, Alireza
Afshari, Ali Taghizadeh
Kheradmand, Fatemeh
Rasmi, Yousef
Sadeghzadeh, Maryam
Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats
title Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats
title_full Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats
title_fullStr Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats
title_full_unstemmed Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats
title_short Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats
title_sort chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6343583/
https://www.ncbi.nlm.nih.gov/pubmed/30713757
http://dx.doi.org/10.1556/1646.10.2018.23
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