The Proliferation,Apoptosis And IL-2 Production Effects Of Modified Acidic Fibroblast Growth Factor On Mouse Spleen Cells

Acid fibroblast growth factor (FGF-1 or FGF-1) is a 17 - 18kDa nonglycosylated polypeptide that is expressed by a variety of cells from all three germ layers. It is a member of FGFs and has extensive biological functions in organ and tissue development, angiogenesis, hematopoiesis, tumorigenesis and wound healing. FGF-1 also has an important effect in immune system. It could significantly enhance the proliferation, apoptosis and cytokine production of T cells caused by antigen stimulation in mice and humans. Aim: This paper mainly explores the effect of modified recombinant human acidic fibroblast growth factor on thymocyte proliferation , apoptosis and IL-2 production in balb/c mice spleens, methods: 1.the proliferation of mouse spleens was measured by [~3H] thymidine incorporation. The experimental groups include: (l)Cells alone, spleen cells cultured in RPM1 medium; (2) FGF-1 (hFGF-1 , rhFGF-1, MrhFGF-1) alone, cells stimulated with FGF-1 alone; (3) ConA alone, cells stimulated with ConA alone; (4)ConA + FGF-1 (hFGF-1 , rhFGF-1 , MrhFGF-1), cells costimulated with FGF-1 added ConA ; 2. 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). 3.The level of IL-2 production is indirectly detected through HT-2 cell proliferation method . the experimental groups is the same to the proliferation experiment's groupsResults: ConA has various mitogenic activities and can stimulate many types of cells to proliferate. FGF-1 alone can not stimulate spleens to proliferate .ConA added hFGF-1 or rhFGF-1 can apparently increase the proliferation level compared to the ConA alone . And wild hFGF-1can costimulate ConA to induce spleens proliferation, but the [~3H]thymidine incorporation induced by MrhFGF-1 added ConA is apparently decreased compare to the hFGF-1or rhFGF-1 added ConA; by analyzing the results of the percentage of apoptosis spleens induced by DEX we know that the percentage of apoptosis pretreated with 100 ng/ml hFGF-1 , rhFGF-1 or MrhFGF-1 was obviously lower than the group treateded with DEX only. further more MrhFGF-1 protects against DEX-induced apoptosis in spleens in dose-dependent manner. by using indirect methods to detect the IL-2 production of spleens, we found that theIL-2 production level induced by MrhFGF-1 add ConA is lower than the wild FGF-1 added ConA, but higher than the levels induced by ConA only.Conclusion: From the [3H]thymidine incorporation experiments results > flow cytometry analysis and the IL-2 production levelwhich was indirectly detected we can guess that the proliferation^ apoptosis protection and IL-2 production signaling induced by the FGF-1 is not the same signal transport.