[2023] PTEN Expression in Progressive (Idiopathic Pulmonary Fibrosis – IPF) Versus Non-Progressive (Sub-Pleural Fibrosis in Recurrent Spontaneous Pneumothorax – RSP) Pulmonary Fibrosis

Rodolfo J Nudelman, Stephanie Schutte, Rongpei Lan, Kevin O Leslie, Jaishree Jagirdar. University of Texas at San Antonio, San Antonio, TX; Mayo Clinic, Scottsdale, AZ

Background: Pro-fibrotic cytokines, Transforming Growth Factor-β (TGF-β) and Platelet Derived Growth Factor (PDGF), secreted by the pulmonary epithelium play a major role in the development of IPF by repressing PTEN expression resulting in smooth muscle actin (SMA) positive myofibroblastic proliferation. PTEN is known to have a role in fibrosis of the liver, kidney, and skin. One of the most enigmatic questions in IPF is the pathogenesis of the progressive fibrosis. The objective of this study is to evaluate PTEN expression in IPF versus non progressive subpleural fibrosis with fibroblastic foci (RSP).
Design: 10 IPF, 5 RSP and 5 normal lung cases (open biopsy or explants) were selected. The slides were stained with hematoxylin and eosin, and immunohistochemical stains for PTEN rabbit monoclonal antibody, (Cell Signaling Technology, Danvers, MA), and SMA mouse monoclonal antibody (Dako, Carpinteria, CA) were performed. A MACH 3 Rabbit HRP Polymer Detection system (Biocare Medical, Concord, CA) was used as a detection system.
Results: In the normal lung, SMA highlighted the muscle fibers within vessels and bronchi, as well as rare interstitial cells. PTEN stained the respiratory epithelium, type 1 and 2 pneumocytes and endothelium. In the RSP cases, SMA and PTEN expression were both strongly positive in subpleural areas of fibrosis. In the IPF cases, SMA showed strong positivity in fibroblastic foci and honeycomb areas while PTEN expression was decreased.
Conclusions: We demonstrate that SMA expression increases while PTEN decreases in IPF in areas of fibroblastic foci and honeycombing; however, in non-progressing fibrosis, SMA and PTEN are strongly coexpressed. Based on these results, we hypothesize that PTEN repression contributes to myofibroblastic differentiation and continued matrix deposition in IPF and may be a key factor in progression.
Category: Pulmonary

Wednesday, March 21, 2012 9:30 AM

Poster Session V # 300, Wednesday Morning

 

Close Window