CAJ | 학술논문

目的观察白血病抑制因子（LIF）受体gp190亚基和gp130亚基胞内区在人白血病细胞系HL-60中与STAT3表达及激活的关系，了解白血病抑制因子（LIF）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-60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pED130/190，LIF诱导10min后，HL-60细胞内的STAT3磷酸化增加（P＜0.01）,经LIF诱导的转染pED130/190的HL-60细胞的STAT3磷酸化水平存在时间依赖性，转染pED190/130的HL-60细胞，LIF诱导6h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LIF诱导下参与HL-60细胞中STAT3的激活。
목적 관찰백혈병억제인자（LIF）수체gp190아기화gp130아기포내구재인백혈병세포계HL-60중여STAT3표체급격활적관계，료해백혈병억제인자（LIF）인발백혈병세포증식억제화분화적궤제。방법 용기인중조기술장gp130화gp190적세포내구호환이구성량개감합체수체기인（130/190,190/130）병분별재HL-60세포표체。용면역조화화면역인적잡교방법분석형성수체아기세포내구동원성이취체후적린산화STAT3적수평화STAT3적표체수평。결과 전염pED130/190，LIF유도10min후，HL-60세포내적STAT3린산화증가（P＜0.01）,경LIF유도적전염pED130/190적HL-60세포적STAT3린산화수평존재시간의뢰성，전염pED190/130적HL-60세포，LIF유도6h후，STAT3적표체강저。결론 백혈병억제인자수체gp190아기세포내구재LIF유도하삼여HL-60세포중STAT3적격활。
Objective To investigate the relation of each subunit of leukemiainhibitory factor(LIFR)and STAT3 in HL-60 for studying the mechanism of leukemia cell proliferateation disorder. Methods We 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. Results As 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.