Lopez-Rivas A, Mendoza S A, Nånberg E, Sinnett-Smith J, Rozengurt E
Proc Natl Acad Sci U S A. 1987 Aug;84(16):5768-72. doi: 10.1073/pnas.84.16.5768.
Addition of the mitogenic peptides bombesin and vasopressin to quiescent Swiss 3T3 mouse cells increased the cytosolic Ca2+ concentration without any measurable delay. In contrast, there was a significant lag period (16 +/- 1.2 s) before platelet-derived growth factor (PDGF) increased cytosolic Ca2+ concentration. This lag was not diminished at high concentrations of either porcine or human PDGF. Similar results were obtained in 3T3 cells loaded with quin-2 or fura-2. The differences in the effects of bombesin, vasopressin, and PDGF on Ca2+ movements were also substantiated by measurements of 45Ca2+ efflux and of cellular 45Ca2+ content. Activation of protein kinase C by phorbol esters inhibited Ca2+ mobilization induced by either bombesin or vasopressin. In contrast, phorbol esters had no effect on PDGF-induced cytosolic Ca2+ concentration increase or acceleration of 45Ca2+ efflux. Finally, bombesin and vasopressin caused a rapid increase in the production of inositol 1,4,5-trisphosphate and inositol 1,3,4-trisphosphate, whereas PDGF, even at a saturating concentration, exerted only a small effect. These results indicate that the signal transduction pathways activated by PDGF that lead to Ca2+ mobilization can be distinguished from those utilized by bombesin and vasopressin.
向静止的瑞士3T3小鼠细胞中添加促有丝分裂肽铃蟾肽和加压素,可使胞质Ca2+浓度升高,且无任何可测量的延迟。相比之下,血小板衍生生长因子(PDGF)升高胞质Ca2+浓度之前存在明显的延迟期(16±1.2秒)。在高浓度的猪或人PDGF作用下,这种延迟并未缩短。在加载了喹啉-2或氟罗-2的3T3细胞中也获得了类似结果。通过测量45Ca2+外流和细胞45Ca2+含量,也证实了铃蟾肽、加压素和PDGF对Ca2+移动的影响存在差异。佛波酯激活蛋白激酶C可抑制铃蟾肽或加压素诱导的Ca2+动员。相比之下,佛波酯对PDGF诱导的胞质Ca2+浓度升高或45Ca2+外流加速没有影响。最后,铃蟾肽和加压素可使肌醇1,4,5-三磷酸和肌醇1,3,4-三磷酸的产生迅速增加,而PDGF即使在饱和浓度下也只有很小的作用。这些结果表明,PDGF激活的导致Ca2+动员的信号转导途径可与铃蟾肽和加压素所利用的途径区分开来。