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Valvular Aortic Stenosis: A Proteomic Insight

Calcified aortic valve disease is a slowly progressive disorder that ranges from mild valve thickening with no obstruction of blood flow, known as aortic sclerosis, to severe calcification with impaired leaflet motion or aortic stenosis. In the present work we describe a rapid, reproducible and effe...

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Autores principales: Gil-Dones, Felix, Martin-Rojas, Tatiana, Lopez-Almodovar, Luis F., de la Cuesta, Fernando, Darde, Veronica M., Alvarez-Llamas, Gloria, Juarez-Tosina, Rocio, Barroso, Gemma, Vivanco, Fernando, Padial, Luis R., Barderas, Maria G.
Formato: Texto
Lenguaje:English
Publicado: Libertas Academica 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884338/
https://www.ncbi.nlm.nih.gov/pubmed/20567634
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author Gil-Dones, Felix
Martin-Rojas, Tatiana
Lopez-Almodovar, Luis F.
de la Cuesta, Fernando
Darde, Veronica M.
Alvarez-Llamas, Gloria
Juarez-Tosina, Rocio
Barroso, Gemma
Vivanco, Fernando
Padial, Luis R.
Barderas, Maria G.
author_facet Gil-Dones, Felix
Martin-Rojas, Tatiana
Lopez-Almodovar, Luis F.
de la Cuesta, Fernando
Darde, Veronica M.
Alvarez-Llamas, Gloria
Juarez-Tosina, Rocio
Barroso, Gemma
Vivanco, Fernando
Padial, Luis R.
Barderas, Maria G.
author_sort Gil-Dones, Felix
collection PubMed
description Calcified aortic valve disease is a slowly progressive disorder that ranges from mild valve thickening with no obstruction of blood flow, known as aortic sclerosis, to severe calcification with impaired leaflet motion or aortic stenosis. In the present work we describe a rapid, reproducible and effective method to carry out proteomic analysis of stenotic human valves by conventional 2-DE and 2D-DIGE, minimizing the interference due to high calcium concentrations. Furthermore, the protocol permits the aortic stenosis proteome to be analysed, advancing our knowledge in this area. SUMMARY: Until recently, aortic stenosis (AS) was considered a passive process secondary to calcium deposition in the aortic valves. However, it has recently been highlighted that the risk factors associated with the development of calcified AS in the elderly are similar to those of coronary artery disease. Furthermore, degenerative AS shares histological characteristics with atherosclerotic plaques, leading to the suggestion that calcified aortic valve disease is a chronic inflammatory process similar to atherosclerosis. Nevertheless, certain data does not fit with this theory making it necessary to further study this pathology. The aim of this study is to develop an effective protein extraction protocol for aortic stenosis valves such that proteomic analyses can be performed on these structures. In the present work we have defined a rapid, reproducible and effective method to extract proteins and that is compatible with 2-DE, 2D-DIGE and MS techniques. Defining the protein profile of this tissue is an important and challenging task that will help to understand the mechanisms of physiological/pathological processes in aortic stenosis valves.
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spelling pubmed-28843382010-06-21 Valvular Aortic Stenosis: A Proteomic Insight Gil-Dones, Felix Martin-Rojas, Tatiana Lopez-Almodovar, Luis F. de la Cuesta, Fernando Darde, Veronica M. Alvarez-Llamas, Gloria Juarez-Tosina, Rocio Barroso, Gemma Vivanco, Fernando Padial, Luis R. Barderas, Maria G. Clin Med Insights Cardiol Methodology Calcified aortic valve disease is a slowly progressive disorder that ranges from mild valve thickening with no obstruction of blood flow, known as aortic sclerosis, to severe calcification with impaired leaflet motion or aortic stenosis. In the present work we describe a rapid, reproducible and effective method to carry out proteomic analysis of stenotic human valves by conventional 2-DE and 2D-DIGE, minimizing the interference due to high calcium concentrations. Furthermore, the protocol permits the aortic stenosis proteome to be analysed, advancing our knowledge in this area. SUMMARY: Until recently, aortic stenosis (AS) was considered a passive process secondary to calcium deposition in the aortic valves. However, it has recently been highlighted that the risk factors associated with the development of calcified AS in the elderly are similar to those of coronary artery disease. Furthermore, degenerative AS shares histological characteristics with atherosclerotic plaques, leading to the suggestion that calcified aortic valve disease is a chronic inflammatory process similar to atherosclerosis. Nevertheless, certain data does not fit with this theory making it necessary to further study this pathology. The aim of this study is to develop an effective protein extraction protocol for aortic stenosis valves such that proteomic analyses can be performed on these structures. In the present work we have defined a rapid, reproducible and effective method to extract proteins and that is compatible with 2-DE, 2D-DIGE and MS techniques. Defining the protein profile of this tissue is an important and challenging task that will help to understand the mechanisms of physiological/pathological processes in aortic stenosis valves. Libertas Academica 2010-02-04 /pmc/articles/PMC2884338/ /pubmed/20567634 Text en © 2010 the author(s), publisher and licensee Libertas Academica Ltd. This is an open access article. Unrestricted non-commercial use is permitted provided the original work is properly cited.
spellingShingle Methodology
Gil-Dones, Felix
Martin-Rojas, Tatiana
Lopez-Almodovar, Luis F.
de la Cuesta, Fernando
Darde, Veronica M.
Alvarez-Llamas, Gloria
Juarez-Tosina, Rocio
Barroso, Gemma
Vivanco, Fernando
Padial, Luis R.
Barderas, Maria G.
Valvular Aortic Stenosis: A Proteomic Insight
title Valvular Aortic Stenosis: A Proteomic Insight
title_full Valvular Aortic Stenosis: A Proteomic Insight
title_fullStr Valvular Aortic Stenosis: A Proteomic Insight
title_full_unstemmed Valvular Aortic Stenosis: A Proteomic Insight
title_short Valvular Aortic Stenosis: A Proteomic Insight
title_sort valvular aortic stenosis: a proteomic insight
topic Methodology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884338/
https://www.ncbi.nlm.nih.gov/pubmed/20567634
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