Shinohara M, Mizuguchi T, Kosaka M, Saito S
First Department of Internal Medicine, School of Medicine, University of Tokushima.
Rinsho Ketsueki. 1991 Nov;32(11):1403-9.
The effect of erythroid differentiation factor (EDF) on the colony formation of erythroid cells (CFU-E and BFU-E) inhibited by the sera from the patients with chronic renal failure (CRF) was evaluated by methylcellulose assay. EDF restored the inhibited formation of CFU-E colony irrespective of the absence or presence of the accessory cells. In addition, EDF was considered to recover BFU-E colony formation through the burst promoting activity (BPA) secreted by the adherent cells. A suicide experiment using 3H-thymidine revealed that EDF acted to induce BFU-E from resting phase to S phase of the cell cycle. Moreover, the number of circulating BFU-E and the secretion of BPA by the mononuclear cells, both of which were significantly low in CRF patients, were also moderately increased by the addition of EDF. These data suggest that EDF could be utilized as a therapeutic agent for pathogenetic factors except hypoproduction of erythropoietin on the anemia of the patients with CRF.
采用甲基纤维素检测法评估了红系分化因子（EDF）对慢性肾衰竭（CRF）患者血清抑制的红系细胞集落形成（CFU-E和BFU-E）的影响。无论是否存在辅助细胞，EDF均可恢复被抑制的CFU-E集落形成。此外，EDF被认为是通过黏附细胞分泌的爆式促进活性（BPA）来恢复BFU-E集落形成。一项使用3H-胸腺嘧啶的自杀实验表明，EDF可促使BFU-E从细胞周期的静止期进入S期。此外，CRF患者循环中BFU-E的数量以及单核细胞分泌的BPA均显著降低，添加EDF后也有适度增加。这些数据表明，对于CRF患者贫血中除促红细胞生成素分泌减少以外的致病因素，EDF可作为一种治疗药物。
