Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2012
IGF-1 alters the human parietal pleural electrochemical profile by inhibiting ion trans-cellular transportation after interaction with its receptor.
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Kouritas Vasileios K, Ioannou Maria, Desimonas Nikolaos, Gourgoulianis Konstantinos I, Molyvdas Paschalis A, Hatzoglou Chrisi
Аннотация
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 μΜ), amiloride 10 μM (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.
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 μΜ), amiloride 10 μM (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.