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MAPK途径在大鼠肝干细胞增殖调控中的作用 |
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【摘要】 目的 探讨ERK1/2、p38-MAPK、PI3K/AKT等信号途径在HGF介导的肝干细胞增殖信号中的作用及其信号转导途径之间的相互联系和作用机制。方法 通过western blotting 检测ERK、 p38MAPK、Akt 信号分子及磷酸化蛋白的表达;通过3H-TdR掺入DNA的方法来检测细胞的增殖细胞。结果 在WB细胞,HGF确实能够激活ERK、 p38MAPK、 PI3K/AKT途径。ERK途径在HGF刺激 5min后发生磷酸化,并且完全磷酸化发生在HGF作用15min,1h后逐渐消失。 Akt 也在HGF作用5min后发生磷酸化,15min后达到完全磷酸化并且持续至少2h。 P38 MAPK 途径也在 5min后开始激活,在 30min后逐渐减少,持续大约3h;我们还发现, 用MAPK抑制剂 U0126, SB23580 处理后能够明显减低HGF诱导的增殖效应, 但是用Ly294002处理阻断PI3K/AKT途径后则并不影响HGF诱导的增殖效应。表明,ERK1/2、p38MAPK 途径的激活参与HGF介导的细胞增殖效应,而PI3K/AKT途径则并不参与HGF介导的细胞增殖调控。结论 在WB细胞,HGF能够激活ERK、 p38MAPK、 PI3K/Akt等信号途径。ERK1/2 和 p38MAPK 途径的激活参与HGF介导的细胞增殖效应,而PI3K/AKT途径则并不参与HGF介导的细胞增殖调控。
【关键词】 肝干细胞; 细胞因子; 信号转导
【Abstract】 Objective To study the role of MAPK and PI3K pathways in hepatocyte growth factor-mediated proliferation effect on WB F-344 cell. Methods To determine effect of HGF on ERK, P38 MAPK, and AKT phosphorylation. Cells were treated or not treated with the specific inhibitors before HGF (40 ng/ml) stimulation, than the phosphorylation of ERK, p38MAPK, Akt following HGF stimulation were analyzed by Western blotting; To determine which pathway involved in HGF induced proliferation activity, proliferation activity were analyzed by [3H] thymidine incorporation. Results The ERK, p38MAPK, Akt pathways were activated by HGF, and involved in mediating cellular proliferation. The proliferation effects of HGF were inhibited when MAPK pathway was abolished by the specific inhibitor U0126, but not inhibited when PI3K/AKT pathway was abolished by inhibitor Ly294002. It suggest that ERK, p38MAPK pathways are involved in HGF-induced proliferation in WB cells. But PI3K/AKT pathways are not involved in HGF-induced proliferation. Conclusion HGF activated ERK, P38 MAPK, and PI3K/AKT pathways; ERK, p38MAPK pathways are involved in HGF-induced proliferation in WB cells. But PI3K/A[1] [2] [3] [4] [5] 下一页
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