摘要
目的:探讨钙敏感受体(calcium-sensing receptor,CaSR)在缺氧诱导的A549及A549/DDP细胞增殖中的信号转导途径。方法:通过缺氧培养箱内(93%N_2、2%O_2、5%CO_2)培养24 h的方法复制细胞缺氧模型。应用Western blot技术分析PCNA及p-AKT蛋白不同处理情况下的表达水平;采用流式细胞技术检测不同处理因素对细胞周期及增殖指数的影响,应用BrdU掺入法分析不同处理因素对细胞DNA合成的影响。结果:缺氧引起A549及A549/DDP细胞PCNA及p-AKT蛋白水平上调,增加BrdU掺入量、S期细胞数量和细胞增殖指数,GdCl_3能够增强缺氧的作用,但上述效应可以被LY294002抑制。结论:PI3K/AKT信号通路在缺氧活化CaSR并促进A549及A549/DDP细胞增殖中起重要作用。
AIM：To explore the cell signal transduction pathway of calcium-sensing receptor （ CaSR） media-ting hypoxia-induced proliferation of A549 cells and A549/DDP cells.METHODS： The cell proliferation was tested by BrdU incorporation assay .The cell cycle analysis was carried out by flow cytometry .The protein levels of PCNA and p-AKT were analyzed by Western blot .RESULTS： Hypoxia significantly increased the protein levels of PCNA and p-AKT, the BrdU incorporation and the cell proliferation index .GdCl3 （ an agonist of CaSR ） amplified the effect of hypoxia .LY294002 （a PI3K inhibitor） decreased the up-regulation of PCNA expression, the BrdU incorporation and the increased cell prolifer-ation index induced by hypoxia and GdCl 3 in the A549 cells and A549/DDP cells.CONCLUSION：CaSR is expressed in A549 cells and 549/DDP cells, and CaSR activation induced by hypoxia promotes the proliferation of A 549 cells and A549/DDP cells through PI3K/AKT signaling pathway .
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2017年第3期505-509,共5页
Chinese Journal of Pathophysiology
基金
齐齐哈尔医学院博士基金资助项目(No.QY2016B-16)
