摘要
目的观察白血病抑制因子 (L IF)受体 gp190亚基和 gp130亚基胞内区在人白血病细胞系 HL- 6 0中与STAT3表达及激活的关系 ,了解白血病抑制因子 (L IF)引发白血病细胞增殖抑制和分化的机制。方法用基因重组技术将gp130和 gp190的细胞内区互换以构成两个嵌合体受体基因 (130 / 190 ,190 / 130 )并分别在 HL- 6 0细胞表达。用免疫组化和免疫印迹杂交方法分析形成受体亚基细胞内区同源性二聚体后的磷酸化 STAT3的水平和 STAT3的表达水平。结果转染p ED130 / 190 ,L IF诱导 10 m in后 ,HL- 6 0细胞内的 STAT3磷酸化增加 (P<0 .0 1) ,经 L IF诱导的转染 p ED130 / 190的 HL- 6 0细胞的 STAT3磷酸化水平存在时间依赖性 ,转染 p ED190 / 130的 HL - 6 0细胞 ,L IF诱导 6 h后 ,STAT3的表达降低。结论白血病抑制因子受体 gp190亚基细胞内区在 L IF诱导下参与 HL- 6 0细胞中 STAT3的激活。
ObjectiveTo investigate the relation of each subunit of leukemia inhibitory factor(LIFR)and STAT3 in HL-60 for studying the mechanism of leukemia cell proliferateation disorder. MethodsWe constructed the chimerical receptor by exchanging the cytoplasmic domain of gp130 and gp190 (130/190,190/130)and expressed it on the membrane of HL-60 Rapid tyrosine phosphorylation of STAT3 and STAT3 level in HL-60 was detected by means of immunoblotting and immunobiochemistry. ResultsAs compared with the group of wild type receptor,higher level of STAT3 expression and rapid phosphorylated STAT3 was found in group of 130/190( P <0 01). We also found that expression of rapid phosphorylated STAT3 in group of 130/190 had a time-dependent manner. Conclusion The result of this study suggest that the cytoplasmic domain of gp190, not gp130, participats in the induction of STAT3 activation in HL-60 [
出处
《免疫学杂志》
CAS
CSCD
北大核心
2001年第3期177-180,共4页
Immunological Journal
基金
国家自然科学基金!资助项目 (396 80 0 12 )
