Koduri P B, Rillema J A
Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201.
Proc Soc Exp Biol Med. 1993 Sep;203(4):424-7. doi: 10.3181/00379727-203-43618.
Studies indicate that G proteins are likely involved in the signal transduction pathway for prolactin's stimulation of mitogenesis in Nb2 cells. In the mammary gland, little is known about the possible role of G proteins in the prolactin (PRL) stimulation of milk product synthesis. Therefore, the effects of cholera and pertussis toxin, enzymes that modify G protein activity, were tested on several actions of prolactin on mouse mammary tissue in culture. At concentration of 0.1-0.5 micrograms/ml, cholera toxin stimulated ornithine decarboxylase activity in a dose-response fashion; when tested in concert, cholera toxin and prolactin caused an additive response. Cholera toxin by itself did not affect the rate of lactose synthesis, but at concentrations above 0.5 micrograms/ml, it attenuated the magnitude of the prolactin stimulation of lactose synthesis. Pertussis toxin (0-0.5 micrograms/ml), both by itself and in concert with PRL, had no effect on ornithine decarboxylase activity. At concentrations of 25 ng/ml and above, pertussis toxin inhibited the PRL stimulation of lactose synthesis, whereas at 0.2 and 0.5 micrograms/ml, pertussis toxin abolished the PRL response. These observations suggest that a G protein, but not Gs, may be involved in prolactin's mechanism of signal transduction in the mouse mammary gland.
研究表明，G蛋白可能参与了催乳素刺激Nb2细胞发生有丝分裂的信号转导途径。在乳腺中，关于G蛋白在催乳素（PRL）刺激乳汁合成过程中可能发挥的作用，人们了解甚少。因此，研究人员检测了可改变G蛋白活性的霍乱毒素和百日咳毒素对培养的小鼠乳腺组织中催乳素的几种作用的影响。霍乱毒素浓度在0.1 - 0.5微克/毫升时，以剂量依赖方式刺激鸟氨酸脱羧酶活性；同时检测时，霍乱毒素和催乳素产生相加效应。单独使用霍乱毒素不影响乳糖合成速率，但浓度高于0.5微克/毫升时，它会减弱催乳素对乳糖合成的刺激幅度。百日咳毒素（0 - 0.5微克/毫升），无论单独使用还是与PRL联合使用，对鸟氨酸脱羧酶活性均无影响。浓度在25纳克/毫升及以上时，百日咳毒素抑制PRL对乳糖合成的刺激作用，而在0.2和0.5微克/毫升时，百日咳毒素则消除PRL反应。这些观察结果表明，一种G蛋白（而非Gs）可能参与了小鼠乳腺中催乳素的信号转导机制。
