Rita S, Michele R, Patrizia O, Alessansdra B, Sara B, Enrico G
Institute of Medical Genetics, University of Ferrara, Italy.
Biochem Mol Biol Int. 1994 Jan;32(1):105-14.
Treatment of PHA-activated PBMC with anti-HLA class I monoclonal antibody (mAb 01.65) shows: 1) depletion of particulate protein Kinase C (PKC) and partial reduction of cytosolic PKC after only 10 min.; 2) inhibition of tritiated thymidine (3H-Td) incorporation; 3) slowing down of cell cycle; 4) reduced expression of four cell cycle related genes. These findings suggest that the depletion of PKC is reflected on the cell cycle progression and expression of cell cycle related genes. We studied, in PHA-activated PBMC cultures, the effect of N-N-Staurosporine (StSp) acting as PKC inhibitor at nanomolar concentrations, alone and combined with mAb 01.65. StSp, inhibits the proliferative response of PHA stimulated PBMC in a competitive fashion with mAb 01.65. We report here that StSp alone and combined with mAb 01.65 affects also the expression of c-myc and cdc2 and the membrane expression of two proliferation markers: IL-2R (CD25) and TfR (CD71).
用抗 HLA I 类单克隆抗体(mAb 01.65)处理PHA激活的外周血单个核细胞(PBMC)显示:1)仅10分钟后,颗粒性蛋白激酶C(PKC)耗竭,胞质PKC部分减少;2)抑制氚标记胸腺嘧啶核苷(3H-Td)掺入;3)细胞周期减慢;4)四个细胞周期相关基因的表达降低。这些发现表明PKC的耗竭反映在细胞周期进程和细胞周期相关基因的表达上。我们在PHA激活的PBMC培养物中研究了纳摩尔浓度下作为PKC抑制剂的N-N-星形孢菌素(StSp)单独作用以及与mAb 01.65联合作用的效果。StSp以与mAb 01.65竞争的方式抑制PHA刺激的PBMC的增殖反应。我们在此报告,单独的StSp以及与mAb 01.65联合使用还会影响c-myc和cdc2的表达以及两种增殖标志物IL-2R(CD25)和TfR(CD71)的膜表达。