Regulation of caveolin-1 membrane trafficking by the Na/K-ATPase

Journal of Cell Biology - Tập 182 Số 6 - Trang 1153-1169 - 2008
Ting Cai1, Haojie Wang2, Yiliang Chen1, Lijun Liu1, William T. Gunning3, Luis Eduardo M. Quintas4, Zijian Xie1,2
11Department of Physiology and Pharmacology
22Department of Medicine,
33Department of Pathology, University of Toledo College of Medicine, Health Science Campus, Toledo, OH 43614
44Departamento de Farmacologia Básica e Clínica, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Cidade Universitária, 21941-902, Rio de Janeiro, Brasil

Tóm tắt

Here, we show that the Na/K-ATPase interacts with caveolin-1 (Cav1) and regulates Cav1 trafficking. Graded knockdown of Na/K-ATPase decreases the plasma membrane pool of Cav1, which results in a significant reduction in the number of caveolae on the cell surface. These effects are independent of the pumping function of Na/K-ATPase, and instead depend on interaction between Na/K-ATPase and Cav1 mediated by an N-terminal caveolin-binding motif within the ATPase α1 subunit. Moreover, knockdown of the Na/K-ATPase increases basal levels of active Src and stimulates endocytosis of Cav1 from the plasma membrane. Microtubule-dependent long-range directional trafficking in Na/K-ATPase–depleted cells results in perinuclear accumulation of Cav1-positive vesicles. Finally, Na/K-ATPase knockdown has no effect on processing or exit of Cav1 from the Golgi. Thus, the Na/K-ATPase regulates Cav1 endocytic trafficking and stabilizes the Cav1 plasma membrane pool.

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Thông tin xuất bản

Journal of Cell Biology

Tập 182 Số 6

1153-1169

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