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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。
OBJECTIVE: To investigate the molecular mechanism by which cholesterol deficiency inhibits the proliferation of Jurkat cells from the perspective of protein tyrosine kinase (PTKs) signal transduction system and cell cycle regulation. Methods Indirect immunofluorescence staining, flow cytometry and immunocytochemical staining were used to do correlation analysis. Results After treated with lovastatin for 3 days, the incorporation rate of 3H-Td R in Jurkat cells cultured in defatted serum medium was significantly decreased, cell proliferation was inhibited, cells were blocked in G0 / G1 phase, PTK activity and cyclin D1, CDK4 protein The expression was significantly reduced, adding L DL can partially reverse the above changes. Conclusions Both endogenous and exogenous cholesterol deficiency can decrease the expression of cyclin D1 and CDK4 protein and decrease the PTK activity in Jurkat cells. It is speculated that this change is directly related to the arrest of G0 / G1 phase and suppression of cell proliferation .