PT  - JOURNAL ARTICLE
AU  - Simona Inghilleri
AU  - Giulia Maria Stella
AU  - Michele Zorzetto
AU  - Ilaria Campo
AU  - Patrizia Morbini
AU  - Tiberio Oggionni
AU  - Maurizio Luisetti
TI  - Phospho-ERM localization in UIP specimens: An immunohistochemystry approach
DP  - 2011 Sep 01
TA  - European Respiratory Journal
PG  - p4773
VI  - 38
IP  - Suppl 55
4099  - http://erj.ersjournals.com/content/38/Suppl_55/p4773.short
4100  - http://erj.ersjournals.com/content/38/Suppl_55/p4773.full
SO  - Eur Respir J2011 Sep 01; 38
AB  - Background: Idiopathic Pulmonary Fibrosis (IPF) is a progressive, fatal lung disease of unknown etiology still lacking of effective therapy. IPF has a poor prognosis with a median survival of 2.5-3.5 years, and it is associated with lung cancer with a prevalence ranging from 4.8% to 48%. Molecular mechanisms of carcinogenesis occurring in IPF remain to be clarified.Aim and objective: The family of ezrin/radixin/moesin (ERM) proteins is essential for maintenance of cell shape, cell adhesion, migration and division, serving as an important cross-linker between the plasma membrane and cytoskeleton. Recent studies showed that ERM is upregulated in multiple types of metastatic cancers. In the current investigation, we tested the hypothesis that ERM interacts and play a key role in epithelial-mesenchimal transition (EMT) in alveolar epithelial cells.Methods: In order to identify the relationship between lung cancer and IPF we assessed an immunohistochemistry analysis for phospho-ERM in the following pulmonary biopsy specimens: 20 IPF/UIP, 4 adenocarcinoma, 6 cryptogenic organizing pneumonia (COP), and 4 normal controls.Results: Our preliminary data showed in normal lung samples a totally negative phospho-ERM immunostaining. We found a weak positivity in COP samples, whereas in UIP samples we found a higher global expression, in particular in activated type II pneumocytes and basal bronchiolar cells.Conclusion: We hypothesize that activation of ERM proteins could be involved in UIP pathogenesis, leading to possible contribute to the EMT process of lung epithelial cells.