Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 281, Issue 1, Pages L79-L85Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.2001.281.1.L79
Keywords
alveolar type II cells; green fluorescent protein; transcriptional regulation; basolateral membrane
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Funding
- NHLBI NIH HHS [HL-65161] Funding Source: Medline
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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 (ERI() 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.
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