Decreased expression of autophagic beclin 1 protein in idiopathic pulmonary fibrosis fibroblasts

Alberto Ricci, Emanuela Cherubini, Davide Scozzi, Vittorio Pietrangeli, Luca Tabbì, Salvatore Raffa, Laura Leone, Vincenzo Visco, Maria Rosaria Torrisi, Pierdonato Bruno, Rita Mancini, Gennaro Ciliberto, Claudio Terzano, Salvatore Mariotta

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)1516-1524
Number of pages9
JournalJournal of Cellular Physiology
Issue number7
Publication statusPublished - Jul 2013

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology


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