Myosin light chain phosphorylation‐dependent modulation of volume‐regulated anion channels in macrovascular endothelium

FEBS Letters

Carton, Iris¹  Eggermont, Jan¹  Walsh, Michael P.³  Bollen, Mathieu²  Nilius, Bernd¹  Prenen, Jean¹  Droogmans, Guy¹ 

[1] Laboratorium voor Fysiologie, Campus Gasthuisberg, Herestraat 49, KU Leuven, B-3000 Leuven, Belgium;Laboratorium voor Biochemie, Campus Gasthuisberg, KU Leuven, B-3000 Leuven, Belgium;Smooth Muscle Research Group and Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, 3330 Hospital Drive N.W., Calgary, Alb. T2N 4N1, Canada

关键词: Chloride channel;    Endothelium;    Cytoskeleton;    Myosin light chain kinase;    Myosin light chain phosphatase;   

DOI  :  10.1016/S0014-5793(00)01097-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The Rho/Rho-associated kinase (ROK) pathway has been shown to modulate volume-regulated anion channels (VRAC) in cultured calf pulmonary artery endothelial (CPAE) cells. Since Rho/ROK can increase myosin light chain phosphorylation, we have now studied the effects of inhibitors of myosin light chain kinase (MLCK) or myosin light chain phosphatase (MLCP) on VRAC in CPAE. Application of ML-9, an MLCK inhibitor, inhibited VRAC, both when applied extracellularly or when dialyzed into the cell. A similar inhibitory effect was obtained by dialyzing the cells with AV25, a specific MLCK inhibitory peptide. Conversely, NIPP1^191–210, an MLCP inhibitory peptide, potentiated the activation of VRAC by a 25% hypotonic stimulus. These data indicate that activation of VRAC is modulated by MLC phosphorylation.

【 授权许可】

Unknown