Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/60084
Title: Barrier-protective effects of activated protein C in human alveolar epithelial cells
Author: Puig, Ferranda
Fuster, Gemma
Adda, Mélania
Blanch, Lluís
Farré Ventura, Ramon
Navajas Navarro, Daniel
Artigas, Antonio
Keywords: Membranes cel·lulars
Cèl·lules epitelials
Proteïnes de membrana
Cell membranes
Epithelial cells
Membrane proteins
Issue Date: 2013
Publisher: Public Library of Science (PLoS)
Abstract: Acute lung injury (ALI) is a clinical manifestation of respiratory failure, caused by lung inflammation and the disruption of the alveolar-capillary barrier. Preservation of the physical integrity of the alveolar epithelial monolayer is of critical importance to prevent alveolar edema. Barrier integrity depends largely on the balance between physical forces on cell-cell and cell-matrix contacts, and this balance might be affected by alterations in the coagulation cascade in patients with ALI. We aimed to study the effects of activated protein C (APC) on mechanical tension and barrier integrity in human alveolar epithelial cells (A549) exposed to thrombin. Cells were pretreated for 3 h with APC (50 mg/ml) or vehicle (control). Subsequently, thrombin (50 nM) or medium was added to the cell culture. APC significantly reduced thrombin-induced cell monolayer permeability, cell stiffening, and cell contraction, measured by electrical impedance, optical magnetic twisting cytometry, and traction microscopy, respectively, suggesting a barrier-protective response. The dynamics of the barrier integrity was also assessed by western blotting and immunofluorescence analysis of the tight junction ZO-1. Thrombin resulted in more elongated ZO-1 aggregates at cell-cell interface areas and induced an increase in ZO-1 membrane protein content. APC attenuated the length of these ZO-1 aggregates and reduced the ZO-1 membrane protein levels induced by thrombin. In conclusion, pretreatment with APC reduced the disruption of barrier integrity induced by thrombin, thus contributing to alveolar epithelial barrier protection.
Note: Reproducció del document publicat a: http://dx.doi.org/10.1371/journal.pone.0056965
It is part of: PLoS One, 2013, vol. 8, num. 2
Related resource: http://dx.doi.org/10.1371/journal.pone.0056965
URI: http://hdl.handle.net/2445/60084
ISSN: 1932-6203
Appears in Collections:Articles publicats en revistes (Ciències Fisiològiques)

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