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中文摘要：
本研究以氯化钆为代表性含稀土元素的化合物，对其在小鼠胚胎成纤维细胞NIH3T3中对蛋白激酶C家族蛋白的激活进行了研究。利用活细胞成像和共聚焦激光扫描技术可以观察到，在血清饥饿的条件下，50μM的氯化钆可以通过增强细胞粘附和细胞骨架重组促进细胞存活。使用蛋白质印迹技术发现蛋白激酶C家族蛋白在氯化钆作用不同时间后可以发生磷酸化，表明蛋白激酶C被激活。此外，双吲哚马来酰亚胺（bisindolylmaleimide，一种PKCpan的抑制剂）可以有效降低PKCpan磷酸化的水平（βⅡSer660），同时也可以降低氯化钆引起的ERK的激活。以上结果表明，氯化钆激活的蛋白激酶C可以通过介导MAPK/ERK信号通路的激活，继而推动细胞周期和细胞存活。
英文摘要：
In the present study, we investigated the activation of protein kinase C （PKC） family in mouse embryonic fibroblast NIH3T3 cells using gadolinium chloride as a representative lanthanide ion. With live cell imaging system and confocal laser scanning microscopy, we found that the treatment of 50 μM GdCI3 promoted cell survival under the condition of serum-starvation. Moreover, better cell attachment and cytoskeleton reorganization were also observed. Additionally, GdC13 treatment resulted in the phosphorylation of PKC family at different time points. Furthermore, bisindolylmaleimide （a PKCpan inhibitor） could efficiently reduce the level of phosphorylated PKCpan （βIISer660）, alleviating ERK activation induced by GdC13. This finding indicated that the PKC activation was involved in GdC13-induced MAPK/ERK signaling and thus might contribute to GdClβ-indueed cell cycle progression and cell survival.
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