摘要
目的：探讨急性早幼粒细胞白血病细胞的分子标志ＰＭＬ－ＲＡＲα在氧化砷（Ａｓ２Ｏ３）诱导的细胞凋亡中的可能作用。方法：观察Ａｓ２Ｏ３对ＰＭＬ－ＲＡＲα蛋白在亚细胞定位的影响。结果：①在１μｍｏｌ／Ｌ的Ａｓ２Ｏ３作用下，ＨＬ－６０细胞核内ＰＭＬ抗血清染色明显减少，而在胞浆的近核膜区出现弥散分布的荧光染色；②Ａｓ２Ｏ３诱导ＮＢ４细胞内散在分布的ＰＭＬ抗血清染色颗粒明显减少；③通常情况下，少数ＮＢ４细胞的胞浆中存在ＰＭＬ抗血清染色颗粒的聚集，这类细胞在Ａｓ２Ｏ３作用后明显增多，凋亡细胞中ＰＭＬ抗血清染色聚集现象也存在；④全反式维甲酸（ＡＴＲＡ）预处理２４或４８小时并不改变Ａｓ２Ｏ３对ＮＢ４细胞的凋亡诱导效应。结论：Ａｓ２Ｏ３诱导细胞凋亡的过程不依赖维甲酸信号途径，可能通过ＰＭＬ／ＰＭＬ－ＲＡＲα及其它相关基因或蛋白的调控来实现。
Objective:In order to illustrate the possible roles of PML RAR α protein in arsenic trioxide(As 2O 3) induced NB4 cell apoptosis.Methods: Effects of As 2O 3 on the subcellular localization of PML RARα in NB4 cells were studied.Results:① Anti PML serum staining was reduced and PML granules emerged in the perinuclear cytoplasm in a diffuse pattern in HL 60 cells under As 2O 3 treatment; ② abnormal PML/PML RAR α granules were decreased;③ NB4 cells accumulated anti PML serum staining granules in the cytoplasms were increased and similar accumulation also found in apoptotic cells;and ④ pretreatment with all trans retinoic acid (ATRA) for 24 or 48 hours did not alter the As 2O 3 effects.Conclusion: As 2O 3 induced apoptosis was independent of the retinoic acid signal pathway,and it might be regulated by PML/PML RAR α and/or other related genes.
出处
《中华血液学杂志》
CAS
CSCD
北大核心
1997年第1期32-34,共3页
Chinese Journal of Hematology
基金
国家自然科学基金
卫生部优秀青年人才基金
上海市科委重点项目
启明星计划
上海血液学研究所胡应洲基金
关键词
氧化砷
蛋白
急性白血病
Arsenic trioxide PML RARα protein Leukemia,myelocytic,acute
