蛋白激酶C对毒胡萝卜素诱导的甲状腺FRTL-5细胞钙内流的调节作用。
Modulatory effect of protein kinase C on thapsigargin-induced calcium entry in thyroid FRTL-5 cells.
作者信息
Törnquist K
机构信息
Endocrine Research Laboratory, University of Helsinki, Minerva Foundation Institute for Medical Research, Finland.
出版信息
Biochem J. 1993 Mar 1;290 ( Pt 2)(Pt 2):443-7. doi: 10.1042/bj2900443.
The aim of the present study was to investigate the regulation of calcium influx in thyroid FRTL-5 cells. Stimulating Fura 2-loaded cells with thapsigargin rapidly increased the cytosolic Ca2+ concentration ([Ca2+]i), which then stabilized at a new elevated plateau level. The initial increase in [Ca2+]i consisted mainly of the release of sequestered Ca2+. The plateau phase was totally dependent on extracellular Ca2+. The influx of Ca2+ was blocked by Ni2+ and was decreased in depolarized cells. The importance of protein kinase C in regulating influx of Ca2+ was then evaluated. Addition of the phorbol ester 12-O-tetradecanoylphorbol 13-acetate prior to thapsigargin significantly decreased the influx of extracellular Ca2+. Studies with bisoxonol to measure membrane potential showed that TPA depolarized the plasma membrane in FRTL-5 cells. In cells where protein kinase C was downregulated or was inhibited by staurosporine, the thapsigargin-induced influx of Ca2+ was enhanced. The results indicate that emptying intracellular Ca2+ pools is sufficient to induce influx of Ca2+ in FRTL-5 cells, and that protein kinase C has a modulatory effect on this process.
本研究的目的是探究甲状腺FRTL-5细胞中钙内流的调节机制。用毒胡萝卜素刺激负载Fura 2的细胞可迅速提高胞质Ca2+浓度（[Ca2+]i），随后其稳定在一个新的升高的平台水平。[Ca2+]i的初始增加主要由储存Ca2+的释放组成。平台期完全依赖于细胞外Ca2+。Ca2+内流被Ni2+阻断，并且在去极化细胞中减少。随后评估了蛋白激酶C在调节Ca2+内流中的重要性。在毒胡萝卜素之前添加佛波酯12-O-十四酰佛波醇13-乙酸酯可显著减少细胞外Ca2+的内流。用双苯甲酰羟肟酸测量膜电位的研究表明，佛波酯可使FRTL-5细胞的质膜去极化。在蛋白激酶C被下调或被星形孢菌素抑制的细胞中，毒胡萝卜素诱导的Ca2+内流增强。结果表明，排空细胞内Ca2+池足以诱导FRTL-5细胞中的Ca2+内流，并且蛋白激酶C对该过程具有调节作用。
Zotero 插件