Yang Kun, Li Qiang
Department of Pediatrics, Teaching Hospital of Chengdu University of TCM, Chengdu 610075, China.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2010 Jul;41(4):630-3.
To Investigate the role of protein kinase C (PKC) signal transduction in the process of HL-60 leukemic cells induced into dendritic cells (DCs) by calcium ionophore A23187.
HL-60 cells were pretreated with protein kinase C (PKC) inhibitor Bis-1 for 24 hours followed by cultured with A23187 for another 36 hours, and the morphology, immunophenotype and function of stimulating proliferation of allogeneic T cells were compared with the cells only treated with A23187.
The morphological changes, surface marker expressions and ability to stimulating the proliferation of allogeneic T cells were inhibited in DCs derived from HL-60 cells treated with PKC inhibitor Bis-1. The percentage of CD83, CD80, CD86 expressing on DCs induced by A23187 significantly decreased to (28.97 +/- 4.05)% vs. (13.23 +/- 2.15)%, (19.10 +/- 5.46)% vs. (9.70 +/- 1.69)%, (41.03 +/- 6.43)% vs. (23.37 +/- 7.50)%, respectively (P < 0.05).
The induction of HL-60 cells induced into DCs by A23187 can be inhibited by PKC inhibitor Bis-1, this suggested that PKC signal transduction pathway might be involved in the process of HL-60 leukemic cells differentiated into DCs by A23187 induction.
探讨蛋白激酶C(PKC)信号转导在钙离子载体A23187诱导HL-60白血病细胞分化为树突状细胞(DCs)过程中的作用。
用蛋白激酶C(PKC)抑制剂Bis-1预处理HL-60细胞24小时,再用A23187培养36小时,将其形态、免疫表型及刺激同种异体T细胞增殖的功能与仅用A23187处理的细胞进行比较。
用PKC抑制剂Bis-1处理的HL-60细胞来源的DCs,其形态变化、表面标志物表达及刺激同种异体T细胞增殖的能力均受到抑制。A23187诱导的DCs上CD83、CD80、CD86的表达百分比显著降低,分别为(28.97±4.05)%对(13.23±2.15)%、(19.10±5.46)%对(9.70±1.69)%、(41.03±6.43)%对(23.37±7.50)%(P<0.05)。
PKC抑制剂Bis-1可抑制A23187诱导HL-60细胞分化为DCs,提示PKC信号转导通路可能参与A23187诱导HL-60白血病细胞分化为DCs的过程。