Decreased expression of autophagic beclin 1 protein in idiopathic pulmonary fibrosis fibroblasts.
J Cell Physiol
; 228(7): 1516-24, 2013 Jul.
Article
em En
| MEDLINE
| ID: mdl-23444126
ABSTRACT
Autophagy is the main cellular pathway for degradation of long-lived proteins and organelles and regulates cell fate in response to stress. Beclin 1 is a key regulator of this process. In some settings autophagy and apoptosis seem to be interconnected. Recent reports indicate that fibroblasts in idiopathic pulmonary fibrosis (IPF) acquire resistance to apoptosis. Here, we examined the expression of beclin 1, and of the anti apoptotic protein Bcl-2 in human IPF fibroblasts using immunohistochemistry and molecular biology in bioptic sections, in primary cultures of fibroblasts taken from patients with IPF and in fibroblast cell lines. Expression of beclin 1 in fibroblasts from IPF was down-regulated in comparison with fibroblasts from normal lungs while the anti-apoptotic protein Bcl-2 expression was over-expressed. Treatment of fibroblast cell cultures with cisplatin induced a significant increase in beclin 1 and caspase 3 protein levels but a reduction in Bcl-2 expression. These observations were confirmed by the analysis of acid compartments and transmission electron microscopy. Our results demonstrate a modified expression of the apoptotic beclin 1 Bcl-2 proteins in human IPF fibroblasts suggesting the existence of an autophagy/apoptosis system dysfunction.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Proteínas Reguladoras de Apoptose
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Fibrose Pulmonar Idiopática
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Proteínas de Membrana
Tipo de estudo:
Observational_studies
/
Risk_factors_studies
Limite:
Female
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Humans
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Male
Idioma:
En
Revista:
J Cell Physiol
Ano de publicação:
2013
Tipo de documento:
Article
País de afiliação:
Itália