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Alveolar Epithelial Type I Cells Express ß2-Adrenergic Receptors and G-protein Receptor Kinase 2

Janice M. Liebler, Zea Borok, Xian Li, Beiyun Zhou, Argelia J. Sandoval, Kwang-Jin Kim and Edward D. Crandall

Will Rogers Institute Pulmonary Research Center, Division of Pulmonary and Critical Care Medicine, University of Southern California, Los Angeles, California

Correspondence to: Janice M. Liebler, MD, Div. of Pulmonary and Critical Care Medicine, U. of Southern California, IRD 620, 2020 Zonal Avenue, Los Angeles, CA 90033. E-mail: liebler{at}usc.edu

ß2-Adrenergic agonists stimulate alveolar epithelial sodium (Na⁺) transport and lung fluid clearance. Alveolar type II (AT2) cells have been reported to express ß2-adrenergic receptors (ß2AR). Given the large surface area covered by alveolar type I (AT1) cells and their potential role in alveolar fluid removal, we were interested in learning if AT1 cells express ß2AR as well. Because ß2AR is potentially susceptible to desensitization by G-protein-coupled receptor kinase 2 (GRK2), we also undertook localization of GRK2. ß2AR and GRK2 expression was evaluated in whole lung, isolated alveolar epithelial cells (AECs), and AECs in primary culture, and was localized to specific AEC phenotypes by immunofluorescence techniques. ß2AR is highly expressed in AT1 cells. ß2AR mRNA increases with time in culture as AT2 cells transdifferentiate towards the AT1 cell phenotype. Immunoreactive GRK2 is seen in both AT1 and AT2 cells in similar amounts. These data suggest that both AT1 and AT2 cells may contribute to the increased alveolar Na⁺ and water clearance observed after exposure to ß2 adrenergic agents. Both cell types also express GRK2, suggesting that both may undergo desensitization of ß2AR with subsequent decline in the stimulatory effects of ß2-adrenergic agonists over time. (J Histochem Cytochem 52:759–767, 2004)

Key Words: alveolar epithelium • ß2-adrenergic receptor • G protein-coupled receptor • kinase 2

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