摘要
目的从蛋白酪氨酸激酶 (PTKs)信号传递系统及细胞周期调控这一角度来探讨胆固醇缺乏抑制 Jurkat细胞增殖的分子机制。方法采用间接免疫荧光染色、流式细胞仪分析技术及免疫细胞化学染色等方法做相关分析。结果经去脂血清培养基培养的 Jurkat细胞加 lovastatin处理 3d后 ,3H- Td R掺入率明显下降 ,细胞增殖受抑 ,细胞受阻于 G0 / G1 期 ,PTK活性及细胞 cyclin D1、CDK4蛋白的表达明显降低 ,加入 L DL 可以部分逆转上述变化。结论无论是内源性还是外源性胆固醇的缺乏都能使 Jurkat细胞 cyclin D1、CDK4蛋白表达降低 ,PTK活性下降 ,推测这一变化与细胞 G0 / G1 期阻滞及细胞增殖受抑有直接关系。
ObjectiveThe molecular mechanisms of cholesterol deficiency on the proliferation of T lymphocytes was investigated from the aspect of protein throsine kinases (PTKs) signal transductions and cell cycle control.Methods[KG-2] 3H TdR incorporation test,indirect immunofluorescent stain,FCM and ICC stain were used in the study.ResultsCellular proliferation was inhibited and blocked on G 0/G 1 phase,the activity of PTKs was decreased and the expression of cyclin D1,CDK4 proteins were down regulated in Jurkat cells after treated with lovastatin for 3d.When treated with LDL,they could partly increased.ConclusionThe decrease of the activity of PTKs and the down regulation of cyclin D1,CDK4 proteins may be related to the effects of cholesterol deficiency on proliferation of Jurkat cells. [
出处
《免疫学杂志》
CAS
CSCD
北大核心
2000年第2期106-109,共4页
Immunological Journal