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This Article Full Text Full Text (PDF) All Versions of this Article: 297/3/L467    most recent 90553.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Cagnina, R. E. Articles by Linden, J. PubMed PubMed Citation Articles by Cagnina, R. E. Articles by Linden, J.

Adenosine A_2B receptors are highly expressed on murine type II alveolar epithelial cells

¹Robert M. Berne Cardiovascular Research Center, Departments of ²Molecular Physiology and Biological Physics and ³Internal Medicine, University of Virginia, Charlottesville, Virginia; and ⁴PGxHealth, LLC, a Division of Clinical Data, Incorporated, Charlottesville, Virginia

Submitted 6 November 2008 ; accepted in final form 1 July 2009

The adenosine A_2B receptor (A_2BR) has a wide tissue distribution that includes fibroblasts and endothelial and epithelial cells. The recent generation of an A_2BR^–/– mouse constructed with a β-galactosidase (β-gal) reporter gene under control of the endogenous promoter has provided a valuable tool to quantify A_2BR promoter activity (29). To determine the sites of expression of the A_2B receptor in the mouse lung, histological and flow cytometric analysis of β-gal reporter gene expression in various lung cell populations was performed. The major site of A_2BR promoter activity was found to be the type II alveolar epithelial cells (AECs), identified by coexpression of prosurfactant protein C, with relatively less expression in alveolar macrophages, bronchial epithelial cells, and cells of the vasculature. Highly purified type II AECs were prepared by fluorescence-activated sorting of enhanced green fluorescent protein (eGFP)-positive cells from transgenic mice expressing eGFP under control of the surfactant protein C promoter (21). The type II cells expressed 89-fold higher A_2BR mRNA than pulmonary leukocytes, and the A_2BR was shown to be functional, as treatment of purified type II AECs with the nonspecific adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) induced an increase in intracellular cAMP greater that the β-adrenergic agonist isoproterenol that was inhibited completely following treatment by ATL-802, a novel, highly potent (K_i = 8.6 nM), and selective (>900 fold over other adenosine receptor subtypes) antagonist of the mouse A_2BR.

lung; β-galactosidase; G protein-coupled receptor; cAMP

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