Teraoka H, Mikoshiba M, Takase K, Yamamoto K, Tsukada K
Department of Pathological Biochemistry, Tokyo Medical and Dental University, Japan.
Exp Cell Res. 1996 Jan 10;222(1):218-24. doi: 10.1006/excr.1996.0027.
We have previously found that dimethyl sulfoxide (DMSO), a known inducer of differentiation in several kinds of myeloid cells, arrests proliferation of human lymphoid cells including Raji and Akata Burkitt's lymphoma cells at the G1 phase. We investigated whether DMSO affects cell proliferation and differentiation of the lymphoid cell line SKW6-CL4, which is capable of differentiating terminally into IgM-producing cells. As in the case of Raji, Akata, and Molt-4, the proliferation of SKW6-CL4 was reversibly arrested at the G1 phase by treatment with 2% DMSO for 5 days even in the presence of interleukin-6 (IL-6). DMSO inhibited spontaneous IgM secretion as well as IL-6-induced IgM production in SKW6-CL4 at a concentration lower than that affecting cell proliferation. Of the cell-surface differentiation markers CD10, CD20, CD21, and CD23, the expression of CD20 was suppressed by DMSO treatment, and partial restoration of the expression was observed 24 to 48 h after release from DMSO. The level of IL-6 receptor protein was not affected by DMSO treatment. These results indicate that DMSO not only arrests the cell cycle of a human lymphoid cell line SKW6-CL4 at the G1 phase but also inhibits the differentiation into IgM-secreting cells at a concentration lower than that affecting cell proliferation and that DMSO overcomes the effect of IL-6 on terminal differentiation of SKW6-CL4. As a whole, proliferation of human lymphoblastoid cell lines was revealed to be reversibly arrested at the G1 phase by DMSO, which is known to induce differentiation in several myeloid cells, without inducing cell differentiation.
我们之前发现,二甲基亚砜(DMSO)是几种髓样细胞中已知的分化诱导剂,可使包括Raji和Akata伯基特淋巴瘤细胞在内的人淋巴细胞增殖停滞于G1期。我们研究了DMSO是否会影响淋巴母细胞系SKW6-CL4的细胞增殖和分化,该细胞系能够终末分化为产生IgM的细胞。与Raji、Akata和Molt-4细胞一样,即使在存在白细胞介素-6(IL-6)的情况下,用2% DMSO处理5天也能使SKW6-CL4细胞的增殖在G1期可逆性停滞。DMSO在低于影响细胞增殖的浓度时,就能抑制SKW6-CL4细胞中自发的IgM分泌以及IL-6诱导的IgM产生。在细胞表面分化标志物CD10、CD20、CD21和CD23中,DMSO处理可抑制CD20的表达,在从DMSO处理中释放24至48小时后可观察到表达的部分恢复。DMSO处理不影响IL-6受体蛋白的水平。这些结果表明,DMSO不仅能使人类淋巴母细胞系SKW6-CL4的细胞周期停滞于G1期,还能在低于影响细胞增殖的浓度时抑制其向分泌IgM细胞的分化,并且DMSO可克服IL-6对SKW6-CL4终末分化的影响。总体而言,已知能诱导几种髓样细胞分化的DMSO可使人类淋巴母细胞系的增殖在G1期可逆性停滞,而不诱导细胞分化。