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Am J Physiol Lung Cell Mol Physiol 281: L79-L85, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 1, L79-L85, July 2001

Dopamine regulates Na-K-ATPase in alveolar epithelial cells via MAPK-ERK-dependent mechanisms

Carmen Guerrero1,2, Emilia Lecuona1, Liuska Pesce1, Karen M. Ridge1, and Jacob I. Sznajder1

1 Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Illinois 60611; and 2 Centro de Investigación del Cáncer, Universidad de Salamanca, 37007 Salamanca, Spain

Dopamine (DA) increases lung edema clearance by regulating vectorial Na+ transport and Na-K-ATPase in the pulmonary epithelium. We studied the role of the mitogen-activated protein kinase (MAPK)-extracellular signal-regulated kinase (ERK) pathway in the DA regulation of Na-K-ATPase in alveolar epithelial cells (AEC). Incubation of AEC with DA resulted in a rapid stimulation of ERK activity via dopaminergic type 2 receptors. Analysis of total RNA and protein showed a 1.5-fold increase in the Na-K-ATPase beta 1-subunit mRNA levels and up to a fivefold increase in beta 1-subunit protein abundance after DA stimulation, which was blocked by the MAPK kinase (MEK) inhibitors PD-98059 and U-0126. Also, the DA-ERK pathway stimulated the synthesis of a green fluorescent protein reporter gene driven by the beta 1-subunit promoter, which indicates that DA regulates the Na-K-ATPase beta 1-subunit at the transcriptional level. The DA-mediated increase in beta 1-subunit mRNA protein resulted in an increase in functional Na pumps in the basolateral membranes of alveolar type II cells. These results suggest that the MAPK-ERK pathway is an important mechanism in the regulation of Na-K-ATPase by DA in the alveolar epithelium.

alveolar type II cells; green fluorescent protein; transcriptional regulation; basolateral membrane


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