FGF-1改构体对小鼠脾细胞增殖与凋亡的影响

Effection of Modified Acidic Fibroblast Growth Factor on Mouse Spleens Proliferation and Apoptosis

目的:主要探讨非促分裂改构人酸性成纤维细胞生长因子(MrhFGF-1)对balb/c小鼠脾细胞增殖和凋亡的影响。方法:采用3H-TdR掺入的方法检测MrhFGF-1同野生型hFGF-1相比对脾细胞增殖的影响,实验组分为(1)对照组;(2)FGF-1处理组;(3)ConA处理组;(4)FGF-1+ConA处理组。用流式细胞仪定量分析MrhFGF-1对脾细胞的凋亡保护作用,(1)对照组;(2)DEX处理组; (3)DEX+FGF-1(hFGF-1、rhFGF-1、MrhFGF-1)处理组。结果表明,利用DNA重组技术构建的一种非促分裂FGF-1突变体MrhFGF-1和野生型FGF-1相比,对脾细胞的促细胞增殖能力明显降低, 但其对细胞凋亡保护作用的影响并无显著性变化,说明FGF-1的促细胞增殖能力和细胞凋亡保护信号通路并非由同一信号通路来实现的。

Objective: The effect of modified acidic fibroblast growth factor (aFGF or FGF-1) on mouse spleens cells proliferation and apoptosis was explored. Methods: The proliferation of mouse spleens was measured by [3H] thymidine incorporation. The experimental groups include:(1) Cells alone, spleens cells cultured in RPM1 medium; (2)FGF-1 alone, cells stimulated with FGF-1 (aFGF) alone; (3)ConA alone, T cells stimulated with ConA alone; (4)ConA + FGF-1, T cells costimulated with both ConA and FGF-1 (aFGF) ; .The apoptosis percentage of spleens induced by dexamethasone was quantitated by flow cytometry. The experimental groups include: (1) controls, spleens cells cultured in RPM1 medium; (2)DEX alone, cells stimulated with DEX alone; (3) DEX + FGF-1 (hFGF-1, rhFGF-1,MrhFGF-1), cells stimulated with DEX+ FGF-1(hFGF-1,rhFGF-1, MrhFGF-1 ). Results: ConA has various mitogenic activities. ConA added hFGF-1 can apparently increase the proliferation compared to the ConA alone in spleens.And wild hFGF-1ean costimulate ConA to induce spleens proliferation, though the [3H] thymidine incorporation induced by MrhFGF-1 added ConA is apparently decreased compare to the hFGF-1 added ConA, through the cytometry analysis results we know that the percentage of apoptosis spleens induced by DEX was obviously lower in those groups pretreated with 100 ng/ml hFGF-1,rhFGF-1 or MrhFGF-1 compared with groups treateded with DEX only. furthermore MrhFGF-1 protects against DEX-induced apoptosis in spleens in dose-dependent manner. Conclusion: From the [3H] thymidine incorporation experiments results and flow cytometry analysis it is possible that the proliferation and apoptosis signaling induced by the FGF-1 is not the same signal transport.