Carlsen S A
Department of Microbiology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
Biochem Cell Biol. 1987 Aug;65(8):710-6. doi: 10.1139/o87-093.
The production of plasminogen activator activity in an auxotrophic mutant of the Chinese hamster ovary cell line was found be greatly stimulated by low concentrations of dimethyl sulfoxide. The production of both cell-associated and excreted plasminogen activator activities was stimulated maximally by dimethyl sulfoxide at a concentration of 2.5%. The stimulation of plasminogen activator activity production was found to be completely inhibited by actinomycin D and cycloheximide but not by mitomycin C, implying that new protein and RNA syntheses were required for this process. Using specific antibodies against plasminogen activator, the presence of a tissue-type plasminogen activator could only be detected in dimethyl sulfoxide treated cells. The dimethyl sulfoxide induced plasminogen activator production was observed only in a mutant auxotrophic for adenosine, glycine, and thymidine but not in wild-type cells. The ability of dimethyl sulfoxide to induce the synthesis of plasminogen activator was lost when the cells were hybridized with another complementary auxotrophic mutant. This implies that the ability of dimethyl sulfoxide to stimulate the production of plasminogen activator may be related to the auxotrophic mutation in this cell.
在中国仓鼠卵巢细胞系的一个营养缺陷型突变体中,发现低浓度的二甲基亚砜能极大地刺激纤溶酶原激活物活性的产生。细胞相关和分泌的纤溶酶原激活物活性的产生在二甲基亚砜浓度为2.5%时受到的刺激最大。发现放线菌素D和环己酰亚胺能完全抑制纤溶酶原激活物活性产生的刺激作用,但丝裂霉素C则不能,这意味着该过程需要新的蛋白质和RNA合成。使用针对纤溶酶原激活物的特异性抗体,仅在经二甲基亚砜处理的细胞中检测到组织型纤溶酶原激活物的存在。二甲基亚砜诱导的纤溶酶原激活物产生仅在对腺苷、甘氨酸和胸苷营养缺陷的突变体中观察到,而在野生型细胞中未观察到。当这些细胞与另一个互补的营养缺陷型突变体杂交时,二甲基亚砜诱导纤溶酶原激活物合成的能力丧失。这意味着二甲基亚砜刺激纤溶酶原激活物产生的能力可能与该细胞中的营养缺陷型突变有关。