Alveolar type II cell‐specific deletion of p120‐catenin in mice demonstrates the crucial role of Type II cell‐localized p120‐ catenin in regulating alveolar epithelial barrier function
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Medientyp:
E-Artikel
Titel:
Alveolar type II cell‐specific deletion of p120‐catenin in mice demonstrates the crucial role of Type II cell‐localized p120‐ catenin in regulating alveolar epithelial barrier function
Beteiligte:
Liu, Yuru;
Reynolds, Albert B;
Malik, Asrar
Beschreibung:
<jats:p>Maintenance of alveolar epithelial barrier integrity is essential for normal alveolar gas exchange function and lung fluid balance. The normal alveolar epithelium is composed of two types of cells: flat type I cells comprising ~95% of the gas‐exchange surface, and cuboidal type II cells, which secrete surfactant. Type II cells also function as facultative progenitor cells in that they can proliferate and trans‐differentiate into type I cells during homeostasis as well as post alveolar epithelial injury. However, molecular mechanisms of maintenance and repair of alveolar barrier are not clear. p120‐ catenin is located at epithelial adherens junction (AJ) where is required for stabilizing E‐Cadherin. Here we addressed whether p120‐catenin contributes to alveolar barrier function in lung. We made an alveolar type II cell specific p120‐Catenin knock‐out mouse line. These mice displayed a persistently leaky alveolar barrier and low grade pulmonary edema and chronic lung inflammation characterized by infiltration of inflammatory cells. These findings indicate that while type II cells make up only 5% of alveolar epithelial surface area, type II cell p120‐catenin plays a critical role in maintenance of alveolar epithelial barrier and homeostasis.</jats:p>