Differential protein expression and basal lamina remodeling in human heart failure.
Proteomics Clin Appl
; 10(5): 585-96, 2016 05.
Article
em En
| MEDLINE
| ID: mdl-26756417
ABSTRACT
PURPOSE:
A goal of this study was to identify and investigate previously unrecognized components of the remodeling process in the progression to heart failure by comparing protein expression in ischemic failing (F) and nonfailing (NF) human hearts. EXPERIMENTALDESIGN:
Protein expression differences were investigated using multidimensional protein identification and validated by Western analysis. This approach detected basal lamina (BL) remodeling, and further studies analyzed samples for evidence of structural BL remodeling. A rat model of pressure overload (PO) was studied to determine whether nonischemic stressors also produce BL remodeling and impact cellular adhesion.RESULTS:
Differential protein expression of collagen IV, laminin α2, and nidogen-1 indicated BL remodeling develops in F versus NF hearts Periodic disruption of cardiac myocyte BL accompanied this process in F, but not NF heart. The rat PO myocardium also developed BL remodeling and compromised myocyte adhesion compared to sham controls. CONCLUSIONS AND CLINICAL RELEVANCE Differential protein expression and evidence of structural and functional BL alterations develop during heart failure. The compromised adhesion associated with this remodeling indicates a high potential for dysfunctional cellular integrity and tethering in failing myocytes. Therapeutically targeting BL remodeling could slow or prevent the progression of heart disease.Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Membrana Basal
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Glicoproteínas de Membrana
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Laminina
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Isquemia Miocárdica
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Colágeno Tipo IV
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Insuficiência Cardíaca
Tipo de estudo:
Prognostic_studies
Limite:
Aged
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Animals
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Humans
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Middle aged
Idioma:
En
Ano de publicação:
2016
Tipo de documento:
Article