Effects of dexamethasone on induction of monocytic differentiation in human U-937 cells by dimethylsulfoxide.

Effects of dexamethasone on induction of monocytic differentiation in human U-937 cells by dimethylsulfoxide.
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地塞米松对二甲基亚砜诱导人 U-937 细胞单核细胞分化的影响。

DOI:
10.1002/jcp.1041420207
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发表时间:
1990
影响因子:
5.6
通讯作者:
Kufe,D
Kufe,D
中科院分区:
生物学2区
文献类型:
--
作者:
Nakamura,T;Kharbanda,S;Spriggs,D;Kufe,D

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目前的研究表明,二甲亚砜 (DMSO) 处理人 U-937 骨髓单核细胞:白血病细胞与单核细胞分化的诱导有关。 DMSO 诱导的 U-937 单核细胞酚型与 (1) 生长抑制、(2) 克隆存活丧失、(3) α-萘乙酸酯酶 (NSE) 染色增加以及 (4) 单核细胞标记 Mac-1 的细胞表面表达增加有关。 U-937 细胞的 DMSO 处理还与 c-myc 和 c-myb 基因表达下调以及肿瘤坏死因子 (TNF) mRNA 水平增加相关。结果进一步证明,DMSO 诱导 U-937 单核细胞分化伴随着磷脂酶 A2 活性的增加。此外,磷脂酶 A2 的这种刺激对地塞米松敏感。因此,我们研究了地塞米松对 DMSO 诱导的 U-937 细胞分化的影响。尽管地塞米松对 DMSO 的生长抑制或克隆存活丧失没有影响,但这种糖皮质激素阻止了 NSE 染色和细胞表面 Mac-1 表达的增加。地塞米松对 c-myc 和 c-m/b 表达的下调也没有影响,但在 DMSO 处理 6 小时后阻止 c-myb 转录物的再现。最后,地塞米松抑制 DMSO 诱导的 TNF 基因表达增加。综上所述,结果表明地塞米松抑制多种特征,包括刺激磷脂酶 A2 活性,与 DMSO 诱导的 U-937 细胞单核细胞分化相关。
The present studies demonstrate that dimethylsulfoxide (DMSO) treatment of human U‐937 myelomonocytic: leukemia cells is associated with induction of monocytic differentiation. The DMSO‐induced U‐937 monocytic phenolype was associated with (1) growth inhibition, (2) loss of clonogenic survival, (3) increases in á‐naphthyl acetate esterase (NSE) staining, and (4) increases in cell surface expression of the monocyte marker Mac‐1. DMSO treatment of U‐937 cells was also associated with down‐regulation of c‐myc and c‐myb gene expression as well as with increases in tumor necrosis factor (TNF) mRNA levels. The results further demonstrate that induction of U‐937 monocytic differentiation by DMSO is accompanied by increases in phospholipase A2activity. Moreover, this stimulation of phospholipase A2was sensitive to dexamethasone. We therefore studied the effects of dexamethasone on DMSO‐induced differentiation of U‐937 cells. Although dexamethasone had no effect on growth inhibition or loss of clonogenic survival by DMSO, this glucocorticoid blocked increases in NSE staining and cell surface Mac‐1 expression. Dexamethasone also had no effect on the down‐regulation of c‐myc and c‐m/b expression but blocked the reappearance of c‐myb transcripts after 6 hr of DMSO treatment. Finally, dexamethasone inhibited DMSO‐induced increases in TNF gene expression. Taken together, the results demonstrate that dexamethasone inhibits multiple characteristics, including the stimulation of phospholipase A2activity, associated with DMSO‐induced monocytic differentiation of U‐937 cells.
DOI: --
发表时间: 1976
期刊: Brain Research
影响因子: 2.9
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DOI: 10.1016/0165-3806(82)90153-5
发表时间: 1982-01-01
期刊: DEVELOPMENTAL BRAIN RESEARCH
影响因子: --
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通讯作者: GREENOUGH, WT
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发表时间: 1972
期刊: The Journal of Physiology
影响因子: --
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DOI: 10.1038/297227a0
发表时间: 1982-01-01
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影响因子: 64.8
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