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J. Biol. Chem., Vol. 281, Issue 47, 36012-36020, November 24, 2006

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A Novel Function of Ionotropic -Aminobutyric Acid Receptors Involving Alveolar Fluid Homeostasis^*

From the Department of Physiological Sciences, Oklahoma State University, Stillwater, Oklahoma 74078

Polarized distribution of chloride channels on the plasma membrane of epithelial cells is required for fluid transport across the epithelium of fluid-transporting organs. Ionotropic -aminobutyric acid receptors are primary ligand-gated chloride channels that mediate inhibitory neurotransmission. Traditionally, these receptors are not considered to be contributors to fluid transport. Here, we report a novel function of -aminobutyric acid receptors involving alveolar fluid homeostasis in adult lungs. We demonstrated the expression of functional ionotropic -aminobutyric acid receptors on the apical plasma membrane of alveolar epithelial type II cells. -Aminobutyric acid significantly increased chloride efflux in the isolated type II cells and inhibited apical to basolateral chloride transport on type II cell monolayers. Reduction of the -aminobutyric acid receptor subunit using RNA interference abolished the -aminobutyric acid-mediated chloride transport. In intact rat lungs, -aminobutyric acid inhibited both basal and agonist-stimulated alveolar fluid clearance. Thus, we provide molecular and pharmacological evidence that ionotropic -aminobutyric acid receptors contribute to fluid transport in the lung via luminal secretion of chloride. This finding may have the potential to develop clinical approaches for pulmonary diseases involving abnormal fluid dynamics.

Received for publication, July 20, 2006 , and in revised form, September 26, 2006.

^* This work was supported in part by National Institutes of Health Grants R01 HL-083188, R01 HL-052146, and R01 HL-071628 and March of Dimes Grant 6FY05-76 (to L. L.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Supported by an American Heart Association Predoctoral Fellowship 0315256Z.

² To whom correspondence should be addressed: 264 McElroy Hall, Stillwater, OK 74078. Tel.: 405-744-4526; Fax: 405-744-8263; E-mail: lin.liu{at}okstate.edu.

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