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首页> 外文期刊>Cellular Signalling >A role for protein kinase C in the regulation of membrane fluidity and Ca~(2+) flux at the endoplasmic reticulum and plasma membranes of HEK293 and Jurkat cells
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A role for protein kinase C in the regulation of membrane fluidity and Ca~(2+) flux at the endoplasmic reticulum and plasma membranes of HEK293 and Jurkat cells

机译：蛋白激酶C在调节HEK293和Jurkat细胞内质网和质膜的膜流动性和Ca〜（2+）通量中的作用

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摘要

Protein kinase C (PKC) plays a prominent role in the regulation of a variety of cellular functions, including Ca~(2+) signalling. In HEK293 and Jurkat cells, the Ca~(2+) release and Ca~(2+) uptake stimulated by several different activators were attenuated by activation of PKC with phorbol myristate acetate (PMA) or 1-oleoyl-2-acetyl-sn-glycerol (OAG) and potentiated by PKC inhibition with G?6983 or knockdown of PKCα or PKCβ using shRNA. Immunostaining and Western blotting analyses revealed that PKCα and PKCβII accumulated at the plasma membrane (PM) and that these isoforms, along with PKCβI, also translocated to the endoplasmic reticulum (ER) upon activation with PMA. Measurements of membrane fluidity showed that, like the cell membrane stabilizers bovine serum albumin (BSA) and ursodeoxycholate (UDCA), PMA and OAG significantly reduced the fluidity of both the PM and ER membranes; these effects were blocked in PKC-knockdown cells. Interestingly, both BSA and UDCA inhibited the Ca~(2+) responses to agonists to the same extent as PMA, whereas Tween 20, which increases membrane fluidity, raised the internal Ca~(2+) concentration. Thus, activation of PKC induces both translocation of PKC to the PM and ER membranes and downregulation of membrane fluidity, thereby negatively modulating Ca~(2+) flux.
机译：蛋白激酶C（PKC）在包括Ca〜（2+）信号传导在内的多种细胞功能的调节中起着重要作用。在HEK293和Jurkat细胞中，通过佛波肉豆蔻酸酯乙酸酯（PMA）或1-油酰基-2-乙酰基-sn激活PKC可以减弱几种不同激活剂刺激的Ca〜（2+）释放和Ca〜（2+）的吸收。 -甘油（OAG），并通过G？6983抑制PKC或使用shRNA敲低PKCα或PKCβ来增强。免疫染色和蛋白质印迹分析显示，PKCα和PKCβII积累在质膜（PM）上，并且这些同种型与PKCβI一起在被PMA激活后也转移到内质网（ER）。膜流动性的测量表明，像细胞膜稳定剂牛血清白蛋白（BSA）和熊去氧胆酸盐（UDCA）一样，PMA和OAG显着降低了PM和ER膜的流动性。这些作用在PKC-nockdown细胞中被阻断。有趣的是，BSA和UDCA都以与PMA相同的程度抑制Ca〜（2+）对激动剂的反应，而Tween 20增加了膜的流动性，从而提高了内部Ca〜（2+）的浓度。因此，PKC的激活既诱导PKC向PM和ER膜移位，又诱导膜流动性下调，从而对Ca〜（2+）通量产生负调节作用。

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