IGF-1 alters the human parietal pleural electrochemical profile by inhibiting ion trans-cellular transportation after interaction with its receptor

Objective: The effect of IGF-1 in the human pleural permeability and the underlying mechanisms involved were investigated. Design: Specimens from thoracic surgical patients were mounted in Ussing chambers. Solutions containing IGF-1 (1 nM-100 nM) and IGF-1 Receptor Inhibitor (1 mu M), amiloride 10 mu M (Na+ channel blocker) and ouabain 1 mM (Na+-K+ pump inhibitor) were used in order to investigate receptor and ion transporter involvement respectively. Trans-mesothelial Resistance (R-TM) across the pleural membrane was determined as a permeability indicator. Immunohistochemistry for IGF-1 receptors was performed. Results: IGF-1 increased R-TM when added on the interstitial surface for all concentrations (p = .008, 1 nM-100 nM) and decreased it on the mesothelial surface for higher concentrations (p = .046, 100 nM). Amiloride and ouabain inhibited this effect. The IGF-1 Receptor Inhibitor also totally inhibited this effect. Immonuhistochemistry demonstrated the presence of IGF-1 receptors in the pleura. Conclusions: It is concluded that IGF-1 changes the electrophysiology of the human parietal pleura by hindering the normal ion transportation and therefore the pleural fluid recycling process. This event is achieved after IGF-1 interaction with its receptor which is present in the human pleura. (C) 2012 Elsevier Ltd. All rights reserved