Differential effects of protein kinase C activation on calcium storage and capacitative calcium entry in NIH 3T3 cells
Differential effects of protein kinase C activation on calcium storage and capacitative calcium entry in NIH 3T3 cells
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DOI：
10.1074/jbc.271.35.21522
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发表时间：
1996-08-30
影响因子：
4.8
通讯作者：
Putney, JW
中科院分区：
文献类型：
--
作者：
Ribeiro, CMP;Putney, JW
在NIH 3T3细胞中，用phorbol 12-肉豆蔻酸13-乙酸酯（PMA）处理可减少thapsigargin释放Ca2+，但不激活Ca2+进入；Ca2+内流是在剩余池被thapsigargin排空后触发的，这种Ca2+内流与对照细胞中由thapsigargin诱导的相似。PMA的作用与Ca2+储存的减少有关，因为1)离子霉素对Ca2+释放的影响与PMA相似，在对照和PMA处理的细胞中，离子霉素在thapsigargin处理后都没有释放Ca2+；2) PMA减少Ca-45（2+）的积累；3) Ca2+指示剂进入内质网的研究表明，PMA减少了储存的Ca2+。虽然PMA本身不激活Ca2+的进入，但PMA通过低浓度的环吡唑酸增强了Ca2+的进入。当环吡唑酸浓度稍高时，PMA对钙的进入没有影响。因此，蛋白激酶C对NIH 3T3细胞中的钙信号传导有两个明显的作用：1)降低细胞内Ca2+储存能力；2)通过细胞内Ca2+池的亚最大消耗来增加钙的进入。这些行为表明蛋白激酶C系统在这种细胞类型的钙稳态中具有复杂和潜在的重要作用。
In NIH 3T3 cells, treatment with phorbol 12-myristate 13-acetate (PMA) reduced the release of Ca2+ by thapsigargin, but did not activate Ca2+ entry; Ca2+ influx was triggered after the residual pool was emptied by thapsigargin, and this Ca2+ influx was similar to that induced by thapsigargin in control cells. The effect of PMA was clue to decreased Ca2+ storage because 1) Ca2+ release by ionomycin was similarly affected by PMA, and in both control and PMA-treated cells, ionomycin did not release Ca2+ following thapsigargin treatment; 2) PMA reduced Ca-45(2+) accumulation; and 3) studies with Ca2+ indicator compartmentalized into the endoplasmic reticulum indicated that stored Ca2+ was reduced by PMA. Although PMA did not itself activate Ca2+ entry, PMA potentiated Ca2+ entry with low concentrations of cyclopiazonic acid. With a somewhat higher concentration of cyclopiazonic acid, PMA had no effect on calcium entry. Thus, protein kinase C has two apparent actions on calcium signaling in NIH 3T3 cells: 1) reduced intracellular Ca2+ storage capacity and 2) augmented calcium entry with submaximal intracellular Ca2+ pool depletion. These actions indicate a complex and potentially important role for the protein kinase C system in calcium homeostasis in this cell type.