Gerhard G S, Phillips P D, Cristofalo V J
Wistar Institute of Anatomy and Biology, Philadelphia, Pennsylvania 19104.
Exp Cell Res. 1991 Mar;193(1):87-92. doi: 10.1016/0014-4827(91)90541-2.
We have examined the ability of epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) to stimulate cultures of young and senescent WI-38 cells to carry out tyrosine-specific phosphorylation of their respective membrane receptors. Previously we reported no reduction in EGF-stimulated phosphorylation in plasma membrane preparations of senescent cells. In this study we found no reduction in PDGF-stimulated phosphorylation in plasma membrane preparations from senescent cells. Furthermore, we found no differences in the EGF- or PDGF-stimulated phosphorylation of their respective receptors in intact cells. These data support the previous findings that although the EGF receptor autokinase activity becomes highly labile during extraction and immunoprecipitation of senescent cells, in situ loss of receptor tyrosine kinase activity is apparently not responsible for the age-associated loss of mitogenic responsiveness.
我们研究了表皮生长因子（EGF）和血小板衍生生长因子（PDGF）刺激年轻和衰老的WI-38细胞培养物，使其各自膜受体进行酪氨酸特异性磷酸化的能力。此前我们报道衰老细胞的质膜制剂中EGF刺激的磷酸化没有降低。在本研究中，我们发现衰老细胞质膜制剂中PDGF刺激的磷酸化也没有降低。此外，我们发现完整细胞中EGF或PDGF刺激其各自受体的磷酸化没有差异。这些数据支持了先前的发现，即尽管在衰老细胞的提取和免疫沉淀过程中EGF受体自身激酶活性变得高度不稳定，但受体酪氨酸激酶活性的原位丧失显然不是有丝分裂反应性随年龄增长而丧失的原因。
