Sawafuji Kanoko, Miyakawa Yoshitaka, Kizaki Masahiro, Ikeda Yasuo
Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Am J Hematol. 2003 Jan;72(1):67-9. doi: 10.1002/ajh.10245.
We studied the effects of cyclosporin A (CsA) on the erythroid differentiation of human erythroid leukemia cell line K562. After K562 was treated with CsA for 4 days, the percentage of hemoglobinized cells was increased by 3.3 times. Because it was reported p38 MAPK (p38) and ERK are involved in erythropoietin-induced erythroid differentiation, we studied their roles using specific inhibitors. p38 inhibitor (SB203580) prevented CsA-induced hemoglobin synthesis in K562 cells, although MEK/ERK inhibitor (U0126) enhanced it by 3.3 times in K562 cells. These results indicate activation of p38 and inactivation of ERK are involved in CsA-induced erythroid differentiation of K562 cells.
我们研究了环孢素A（CsA）对人红白血病细胞系K562红系分化的影响。用CsA处理K562细胞4天后，血红蛋白化细胞的百分比增加了3.3倍。由于有报道称p38丝裂原活化蛋白激酶（p38）和细胞外信号调节激酶（ERK）参与促红细胞生成素诱导的红系分化，我们使用特异性抑制剂研究了它们的作用。p38抑制剂（SB203580）可阻止CsA诱导K562细胞中的血红蛋白合成，而MEK/ERK抑制剂（U0126）在K562细胞中可使其增强3.3倍。这些结果表明，p38的激活和ERK的失活参与了CsA诱导的K562细胞红系分化。
