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Caveolin-1 is involved in high glucose accelerated human glomerular mesangial cell senescence

BACKGROUND/AIMS: We demonstrated the role of caveolin-1 involved in high glucose (HG)-induced glomerular mesangial cells (GMCs) senescence. METHODS: HG was used to stimulate GMCs. The telomere lengths were analyzed by Southern blot. β-Galactosidase staining was determined. The expressions of caveoli...

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Detalles Bibliográficos
Autores principales: Feng, Xin, Gao, Wei, Li, Yao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Association of Internal Medicine 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583444/
https://www.ncbi.nlm.nih.gov/pubmed/27048255
http://dx.doi.org/10.3904/kjim.2015.254
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author Feng, Xin
Gao, Wei
Li, Yao
author_facet Feng, Xin
Gao, Wei
Li, Yao
author_sort Feng, Xin
collection PubMed
description BACKGROUND/AIMS: We demonstrated the role of caveolin-1 involved in high glucose (HG)-induced glomerular mesangial cells (GMCs) senescence. METHODS: HG was used to stimulate GMCs. The telomere lengths were analyzed by Southern blot. β-Galactosidase staining was determined. The expressions of caveolin-1 and P53 proteins were determined by Western blot. RESULTS: Treatment with high concentrations of glucose induced GMC senescence accompanied by shortened telomere length and increase of β-galactosidase staining as well as P53 protein, which was abrogated after application of caveolin-1-siRNA. CONCLUSIONS: This study proved that HG induced cell senescence in GMCs. The caveolin-1 is involved in HG-induced mesangial cell senescence, and blocking caveolin-1 significantly reduced cell senescence. The effect of caveolin-1 is mediated by P53 pathway.
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spelling pubmed-55834442017-09-05 Caveolin-1 is involved in high glucose accelerated human glomerular mesangial cell senescence Feng, Xin Gao, Wei Li, Yao Korean J Intern Med Original Article BACKGROUND/AIMS: We demonstrated the role of caveolin-1 involved in high glucose (HG)-induced glomerular mesangial cells (GMCs) senescence. METHODS: HG was used to stimulate GMCs. The telomere lengths were analyzed by Southern blot. β-Galactosidase staining was determined. The expressions of caveolin-1 and P53 proteins were determined by Western blot. RESULTS: Treatment with high concentrations of glucose induced GMC senescence accompanied by shortened telomere length and increase of β-galactosidase staining as well as P53 protein, which was abrogated after application of caveolin-1-siRNA. CONCLUSIONS: This study proved that HG induced cell senescence in GMCs. The caveolin-1 is involved in HG-induced mesangial cell senescence, and blocking caveolin-1 significantly reduced cell senescence. The effect of caveolin-1 is mediated by P53 pathway. The Korean Association of Internal Medicine 2017-09 2016-04-06 /pmc/articles/PMC5583444/ /pubmed/27048255 http://dx.doi.org/10.3904/kjim.2015.254 Text en Copyright © 2017 The Korean Association of Internal Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Feng, Xin
Gao, Wei
Li, Yao
Caveolin-1 is involved in high glucose accelerated human glomerular mesangial cell senescence
title Caveolin-1 is involved in high glucose accelerated human glomerular mesangial cell senescence
title_full Caveolin-1 is involved in high glucose accelerated human glomerular mesangial cell senescence
title_fullStr Caveolin-1 is involved in high glucose accelerated human glomerular mesangial cell senescence
title_full_unstemmed Caveolin-1 is involved in high glucose accelerated human glomerular mesangial cell senescence
title_short Caveolin-1 is involved in high glucose accelerated human glomerular mesangial cell senescence
title_sort caveolin-1 is involved in high glucose accelerated human glomerular mesangial cell senescence
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583444/
https://www.ncbi.nlm.nih.gov/pubmed/27048255
http://dx.doi.org/10.3904/kjim.2015.254
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