Involvement of phospholipase D in store‐operated calcium influx in vascular smooth muscle cells

FEBS Letters

Tepel, Martin¹  Assmann, Gerd²  Nofer, Jerzy-Roch²  Neusser, Markus¹  Walter, Michael²  Zidek, Walter¹ 

[1] Medizinische Universitätsklinik, Marienhospital Herne, Herne, Germany;Institut für Arterioskleroseforschung, Universität Münster, Münster, Germany

关键词: Calcium;    Phospholipase D;    Signal transduction;    Thapsigargin;    Bradykinin;    Phosphatidylinositol;    Phosphatidylcholine;    [Ca2+]i;    intracellular free calcium concentration;    DG;    1;    2-diacylglycerol;    InsP3;    inositol 1;    4;    5-trisphosphate;    PA;    phosphatidic acid;    PBS;    phosphate-buffered saline;    PBut;    phosphatidylbutanol;    PC;    phosphatidylcholine;    PLC;    phospholipase C;    PLD;    phospholipase D;    PIP2;    phosphatidylinositol 4;    5-bisphosphate;    PIP;    phosphatidylinositol 4-monophosphate;    PI;    phosphatidylinositol;    VSMC;    vascular smooth muscle cells;   

DOI  :  10.1016/S0014-5793(00)01880-9

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

In non-excitable cells, sustained intracellular Ca²⁺ increase critically depends on influx of extracellular Ca²⁺. Such Ca²⁺ influx is thought to occur by a ‘store-operated’ mechanism, i.e. the signal for Ca²⁺ entry is believed to result from the initial release of Ca²⁺ from inositol 1,4,5-trisphosphate-sensitive intracellular stores. Here we show that the depletion of cellular Ca²⁺ stores by thapsigargin or bradykinin is functionally linked to a phosphoinositide-specific phospholipase D (PLD) activity in cultured vascular smooth muscle cells (VSMC), and that phosphatidic acid formed via PLD enhances sustained calcium entry in this cell type. These results suggest a regulatory role for PLD in store-operated Ca²⁺ entry in VSMC.

【 授权许可】

Unknown