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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。
In this study, gadolinium chloride as a representative compounds containing rare earth elements, its protein kinase C family protein activation in mouse embryonic fibroblasts NIH3T3 were studied. Using live cell imaging and confocal laser scanning techniques, it was observed that 50 μM gadolinium chloride promoted cell survival by enhancing cell adhesion and cytoskeletal reorganization under serum starved conditions. Using Western blotting, it was found that the protein kinase C family of proteins phosphorylated at different times after gadolinium chloride treatment, indicating that protein kinase C is activated. In addition, bisindolylmaleimide (an inhibitor of PKCpan) can effectively reduce the level of PKCpan phosphorylation (βIISer660), but also can reduce the ERK activation caused by gadolinium chloride. These results suggest that gadolinium chloride-activated protein kinase C can promote cell cycle and cell survival by mediating the activation of MAPK / ERK signaling pathway.