Uchino S
Nihon Sanka Fujinka Gakkai Zasshi. 1981 Nov;33(11):1961-70.
It has been observed that the surface charge of cells may increase during cell multiplication. Therefore, the studies were performed to investigate the cytopathogenesis of the endometrial abnormal proliferation by tracing cell microelectrophoretic changes. The studies consist of: 1. The comparison of surface charges on cells between proliferative and secretory phases of endometrium. 2. Changes of the surface charge in cases of the endometrial cells after curretage, and of cystic hyperplasia and/or differentiated adenocarcinoma of endometrium. 3. Those hormonal effects on cell surface charge as estrogen, progesterone, testosterone and cortisol on cases above mentioned in vivo and in vitro. 4. Relationship between electric charge and sialic acid on cell surface. 5. Quantitative variation of sialic acid on cell surface when those hormonal agents were applied. The results were as follows: 1. The negative charge on endometrial cell surface increased according to the cell proliferation and decreased in differentiation. 2. Estrogen usually increased the surface charge while progesterone decreased it in both normal and abnormal states of the endometrium, in both in vivo and in vitro experiments. Testosterone showed effects similar to those of progesterone, while no cortisol affected the surface charge density of endometrial cells. 3. Sialic acid were even more in cases of higher surface charge on cells. 4. Estrogen increased sialic acid an progesterone decreased it. Testosterone showed similar effects to progesterone and cortisol did not affect the sialic acid quantity. 5. Anticarcinogenic agents generally decreased the electric charge of cell surface. As a result, it was known that the density of surface charge on endometrial cells determined by cell microelectrophoresis increased in cell proliferation and decreased in differentiation of endometrial cells. Those variation may depend upon some steroid hormones such as estrogen or progesterone.
据观察,细胞表面电荷可能在细胞增殖过程中增加。因此,开展了相关研究以通过追踪细胞微电泳变化来探究子宫内膜异常增殖的细胞发病机制。这些研究包括:1. 子宫内膜增殖期与分泌期细胞表面电荷的比较。2. 刮宫后子宫内膜细胞、子宫内膜囊性增生和/或分化型腺癌病例中细胞表面电荷的变化。3. 雌激素、孕激素、睾酮和皮质醇等激素在体内和体外对上述病例细胞表面电荷的影响。4. 细胞表面电荷与唾液酸之间的关系。5. 应用这些激素制剂时细胞表面唾液酸的定量变化。结果如下:1. 子宫内膜细胞表面负电荷随细胞增殖而增加,随分化而减少。2. 在子宫内膜的正常和异常状态下,无论是体内还是体外实验,雌激素通常会增加表面电荷,而孕激素则会降低表面电荷。睾酮显示出与孕激素类似的作用,而皮质醇对子宫内膜细胞的表面电荷密度没有影响。3. 细胞表面电荷较高的病例中唾液酸含量更高。4. 雌激素增加唾液酸,孕激素降低唾液酸。睾酮显示出与孕激素类似的作用,皮质醇不影响唾液酸含量。5. 抗癌剂通常会降低细胞表面电荷。结果表明,通过细胞微电泳测定的子宫内膜细胞表面电荷密度在细胞增殖时增加,在子宫内膜细胞分化时降低。这些变化可能取决于一些类固醇激素,如雌激素或孕激素。