β‐Agonists regulate Na,K‐ATPase via novel MAPK/ERK and rapamycin‐sensitive pathways

FEBS Letters

Comellas, Alejandro¹  Pesce, Liuska¹  Ridge, Karen M.¹  Sznajder, Jacob I.¹  Guerrero, Carmen¹ 

[1] Division of Pulmonary and Critical Care Medicine, Northwestern University, 300 E. Superior St., Tarry Building 14-707, Chicago, IL 60611, USA

关键词: Isoproterenol;    cAMP;    Protein kinase A;    Mammalian target of rapamycin;    Lung;    ISO;    isoproterenol;    AEC;    alveolar epithelial cell;    MAPK;    mitogen-activated protein kinases;    ERK;    extracellular signaling related kinases;    mTOR;    mammalian target of rapamycin;    PKA;    protein kinase A;    BLM;    basolateral membrane;   

DOI  :  10.1016/S0014-5793(00)02298-5

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

We studied whether the β-adrenergic agonist, isoproterenol (ISO), regulates Na,K-ATPase in alveolar epithelial cells (AEC) via a mitogen-activated protein kinase (MAPK)/extracellular signaling related kinase (ERK) dependent pathway. ISO increased ERK activity in AEC by 10 min via a β-adrenergic receptor, protein kinase A (PKA)-dependent mechanism. Activation of the MAPK pathway by ISO, resulted in increased Na,K-ATPase β1 and α1 subunit protein abundance in whole cell lysates, which resulted in functional Na,K-ATPases at the basolateral membranes. ISO did not change the α1 or β1 mRNA steady state levels, but rapamycin, the inhibitor of the mammalian target of rapamycin, also blocked the ISO-mediated increase in Na,K-ATPase total protein abundance, suggesting a posttranscriptional regulation. We conclude that ISO, regulates the Na,K-ATPase in AEC via PKA, ERK and rapamycin-sensitive mechanisms.

【 授权许可】

Unknown