Calcium release-activated calcium (CRAC) channels mediate the β2-adrenergic regulation of Na,K-ATPase |
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| Institution: | 1. Division of Pulmonary and Critical Care Medicine, Department of Medicine, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA;2. Department of Molecular Pharmacology and Biological Chemistry, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA |
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| Abstract: | β2-Adrenergic agonists have been shown to regulate Na,K-ATPase in the alveolar epithelium by recruiting Na,K-ATPase-containing vesicles to the plasma membrane of alveolar epithelial cells (AEC). Here, we provide evidence that β2-agonists induce store-operated calcium entry (SOCE) in AECs. This calcium entry is necessary for β2-agonist-induced recruitment of Na,K-ATPase to the plasma membrane of AECs. Specifically, we show that β2-agonists induce SOCE via stromal interaction molecule 1 (STIM1)-associated calcium release-activated calcium (CRAC) channels. We also demonstrate that the magnitude of SOCE affects the abundance of Na,K-ATPase at the plasma membrane of AECs. |
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| Keywords: | Calcium channel Calcium signaling Store-operated calcium entry Epithelial cell Na K-ATPase |
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