Influence Of JNK Signal On Jurkat T Cell Apoptosis Induced By Anisomycin

Objective:To study possible interaction mechanisms of JNK signaling on apoptosis of Jurkat T cell induced by Anisomycin.Methods:DNA ladder was used to measure effects of Anisomycin on the apoptosis of Jurkat T cell at different times. With Flow Cytometry, we investigated Jurkat T cell apoptosis induced by Anisomycin at different times and the reverse effect of SP600125 on it. By Western Blot, expressions of ERK1/2, P-ERK1/2, JNK1/2, P-JNK1/2, p38 and P-p38 were examined to study interfering effects of PD98059, SP600125 and SB203580 on MAPK pathway, and then interrelationships of ERK1/2, JNK1/2 and p38 signals in Jurkat T cell death induced by different concentrations of Anisomycin were analyzed. Focusing on the JNK1/2 pathway in Jurkat T cells, expression levels of P-BCL-XL and P-BIM pro-teins were detected throuth Western Blot, and levels of BCL-XL and BIM mRNA were examined by RT-PCR for further confirmation. Results:DNA fracture frag-ments were increased as the enhancement of stimulating time (0-6 h) and concentra-tion (5-80 ng/ml) of Anisomycin in time-and dose-dependent manners. Anisomycin suppressed the expression of P-ERK1/2 in a dose-dependent manner, appearing the most significant at 3 h, but the expression of ERK1/2 showed no significant difference. Anisomycin stimulated the expressions of P-p38 and P-JNK1/2 in a dose-dependent manner. On the contrary the levels of p38 and JNK1/2 were not changed significantly. SP600125 inhibited the expression of P-JNK1/2 in Jurkat T cells induced by Aniso-mycin, but PD98059 and SB203580 could not do. Anisomycin could induce the expressions of P-BCL-XL in Jurkat T cells dose-dependently with stimulating time prolonged. Anisomycin could induce the expressions of P-BIM in a dose-dependent manner. The expression of BIM mRNA was up-regulated with increased concentra-tions of Anisomycin, while the expression of BCL-XL mRNA was dow-regulated with the same stimulus. Conclusion:Anisomycin may induce the apoptosis of Jurkat T cells significantly via JNK-BCL-XL/JNK-BIM signal pathways.