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Am J Physiol Lung Cell Mol Physiol (December 16, 2005). doi:10.1152/ajplung.00373.2005
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Submitted on August 25, 2005
Accepted on December 14, 2005

Adenosine A2A Receptors Promote Adenosine-stimulated Wound Healing in Bronchial Epithelial Cells

D S Allen-Gipson1*, J Wong1, J R Spurzem2, J H Sisson1, and T A Wyatt2

1 Pulmonary, Critical Care & Sleep Medicine Section, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, USA
2 Pulmonary, Critical Care & Sleep Medicine Section, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, USA; Research Service, Department of Veterans Affairs, Omaha, NE, USA

* To whom correspondence should be addressed. E-mail: dallengipson{at}unmc.edu.

Adenosine produces a wide variety of physiological effects through the activation of specific adenosine receptors (A1, A2A, A2B, A3). Adenosine, acting particularly at the A2A adenosine receptor (A2AAR), is a potent endogenous anti-inflammatory agent and sensor of excessive inflammatory tissue damage. The complete healing of wounds is the final step in a highly regulated response to injury. Recent studies on epidermal wounds have identified the A2AAR as the main adenosine receptor responsible for altering the kinetics of wound closure. We hypothesized that A2AAR promotes wound healing in bronchial epithelial cells (BECs). To test this hypothesis, the human epithelial cell line (BEAS-2B) and bovine bronchial epithelial cells (BBECs) were used. Real-time RT-PCR of RNA from unstimulated BEAS-2B revealed transcriptional expression of A1, A2A, A2B and A3 receptors. Western Blot analysis of lysates from BEAS-2B and BBEC cells detected a single band at 44.7 kDa in both the BECs indicating the presence of A2AAR. In a wound-healing model, we found that adenosine stimulated wound repair in cultured BBECs in a concentration-dependent manner with an optimal closure rate observed between 4-6 hours. Similarly, the A2AAR agonist 5'-(N-cyclopropyl) carboxamidoadenosine (CPCA) augmented wound closure with a maximal closure rate occurring between 4-6 hr. Inhibition of A2AAR with ZM241385, a known A2AAR antagonist, impeded wound healing. In addition, ZM241385 also attenuated adenosine-mediated wound repair. Kinase studies revealed adenosine-stimulated airway repair activates protein kinase A (PKA) via ligating A2AAR. Collectively, the data suggest that the A2AAR is involved in BEC adenosine-stimulated wound healing and may prove useful in understanding purinergic-mediated actions on airway epithelial repair.




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