We investigated the distribution of alpha-skeletal, alpha-cardiac, and alpha-smooth muscle actin isoforms in human heart during development, hypertrophy, and failure. At 20 weeks of fetal life, alpha-skeletal actin was localized in a small proportion of subendocardial and papillary muscle cardiomyocytes. At this gestation time, diffuse alpha-cardiac actin staining was observed, associated with focal expression of alpha-smooth muscle actin. In normal adult subjects, alpha-skeletal actin positive cardiomyocytes were distributed in a transmural gradient with the highest proportion located subendocardially. In myocardial hypertrophy and cardiomyopathies, the amount of alpha-skeletal actin was increased and diffuse staining was seen in all layers of ventricular myocardium, with the exception of idiopathic dilated cardiomyopathies. Cardiomyocytes were negative for of-smooth muscle actin in all pathological situations studied. As expected, fibroblasts in post-infarct scars expressed of smooth muscle actin and transforming growth factor-beta1 but, surprisingly, were negative for these proteins in interstitial fibrosis. Our results demonstrate that increased expression of alpha-skeletal actin in the diseased human heart is associated with increased myocyte stretch, increased wall stress, and pressure overload, but not with idiopathic dilated cardiomyopathies. They also suggest that fibrotic changes develop with different mechanisms in scars versus interstitial fibrosis. Copyright (C) 2003 John Wiley Sons, Ltd.

Suurmeijer, A., Clement, S., Francesconi, A., Bocchi, L., Angelini, A., Van Veldhuisen, D., et al. (2003). Alpha-actin isoform distribution in normal and failing human heart: a morphological, morphometric, and biochemical study. JOURNAL OF PATHOLOGY, 199(3), 387-397 [10.1002/path.1311].

Alpha-actin isoform distribution in normal and failing human heart: a morphological, morphometric, and biochemical study

SPAGNOLI, LUIGI GIUSTO;ORLANDI, AUGUSTO
2003-01-01

Abstract

We investigated the distribution of alpha-skeletal, alpha-cardiac, and alpha-smooth muscle actin isoforms in human heart during development, hypertrophy, and failure. At 20 weeks of fetal life, alpha-skeletal actin was localized in a small proportion of subendocardial and papillary muscle cardiomyocytes. At this gestation time, diffuse alpha-cardiac actin staining was observed, associated with focal expression of alpha-smooth muscle actin. In normal adult subjects, alpha-skeletal actin positive cardiomyocytes were distributed in a transmural gradient with the highest proportion located subendocardially. In myocardial hypertrophy and cardiomyopathies, the amount of alpha-skeletal actin was increased and diffuse staining was seen in all layers of ventricular myocardium, with the exception of idiopathic dilated cardiomyopathies. Cardiomyocytes were negative for of-smooth muscle actin in all pathological situations studied. As expected, fibroblasts in post-infarct scars expressed of smooth muscle actin and transforming growth factor-beta1 but, surprisingly, were negative for these proteins in interstitial fibrosis. Our results demonstrate that increased expression of alpha-skeletal actin in the diseased human heart is associated with increased myocyte stretch, increased wall stress, and pressure overload, but not with idiopathic dilated cardiomyopathies. They also suggest that fibrotic changes develop with different mechanisms in scars versus interstitial fibrosis. Copyright (C) 2003 John Wiley Sons, Ltd.
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/08 - Anatomia Patologica
English
Con Impact Factor ISI
alpha-skeletal actin; alpha-cardiac actin; alpha-smooth muscle actin; heart development; hypertrophy; idiopathic dilated cardiomyopathy
Suurmeijer, A., Clement, S., Francesconi, A., Bocchi, L., Angelini, A., Van Veldhuisen, D., et al. (2003). Alpha-actin isoform distribution in normal and failing human heart: a morphological, morphometric, and biochemical study. JOURNAL OF PATHOLOGY, 199(3), 387-397 [10.1002/path.1311].
Suurmeijer, A; Clement, S; Francesconi, A; Bocchi, L; Angelini, A; Van Veldhuisen, D; Spagnoli, Lg; Gabbiani, G; Orlandi, A
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/50063
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