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1 Medicine, Univ Minnesota, Minneapolis, Minnesota, United States
2 Environmental Health Science, SPH, Univ Minnesota, Minneapolis, Minnesota, United States
* To whom correspondence should be addressed. E-mail: ingba001{at}umn.edu.
Thyroid hormone (T3) increases Na,K-ATPase activity in rat adult alveolar type II cells via a PI3K-dependent pathway. In these cells, dopamine and 
-adrenergic agonists can stimulate Na,K-ATPase activity through either PI3K or MAPK pathways. We assessed the role of the MAPK pathway in the stimulation of Na,K-ATPase by T3. In the adult rat alveolar type II - like cell line MP48, T3 enhanced MAPK/ERK1/2 activity in a dose-dependent manner. Increased ERK1/2 phosphorylation was observed within 5 minutes, peaked at 20 minutes and then decreased. Two MEK1/2 inhibitors, U0126 and PD98059, each abolished the T3 - induced increase in the quantity of Na,K-ATPase alpha-1 subunit plasma membrane protein and Na, K-ATPase activity. T3 also increased the phosphorylation of MAPK/p38, however, SB203580, a specific inhibitor of MAPK/p38 activity did not prevent the T3-induced Na, K-ATPase activity. SP600125, a specific inhibitor of the MAPK/JNK pathway, also did not block the T3 - induced Na, K-ATPase activity. Phorbol-12-myristate-13-acetate (PMA) significantly increased ERK1/2 phosphorylation and Na,K-ATPase activity. The PMA-induced Na,K-ATPase activity was inhibited by U0126. These data indicate that activation of MAPK-ERK1/2 was required for the T3-induced increase in Na, K-ATPase activity in addition to the requirement for the PI3K pathway.
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