Kawahara Y, Kariya K, Araki S, Fukuzaki H, Takai Y
Department of Internal Medicine (1st Division), Kobe University School of Medicine, Japan.
Biochem Biophys Res Commun. 1988 Oct 31;156(2):846-54. doi: 10.1016/s0006-291x(88)80921-5.
In cultured rabbit vascular smooth muscle cells (VSMC), platelet-derived growth factor (PDGF), a potent mitogen for VSMC, induced the dose- and time-dependent formation of inositol mono-, bis- and trisphosphates (IP1, IP2 and IP3, respectively). The doses of PDGF necessary for these reactions were similar to those for DNA synthesis. The maximal level of IP1 was comparable to, and those of IP2 and IP3 were about half of those induced by angiotensin II, a potent vasoconstrictor. However, the time courses of the PDGF-induced reactions were slower than those of the angiotensin II-induced ones. Moreover, protein kinase C-activating phorbol esters inhibited the angiotensin II-induced reactions, but did not the PDGF-induced ones. These results indicate that PDGF induces the phospholipase C reactions in VSMC but suggest that the signaling mechanism of PDGF to the phospholipase C is different from that of angiotensin II.
在培养的兔血管平滑肌细胞（VSMC）中，血小板衍生生长因子（PDGF）是一种对VSMC有强大促有丝分裂作用的因子，它能诱导肌醇单磷酸、双磷酸和三磷酸（分别为IP1、IP2和IP3）呈剂量和时间依赖性形成。这些反应所需的PDGF剂量与DNA合成所需剂量相似。IP1的最大水平与血管紧张素II（一种强大的血管收缩剂）诱导的水平相当，而IP2和IP3的最大水平约为血管紧张素II诱导水平的一半。然而，PDGF诱导反应的时间进程比血管紧张素II诱导反应的时间进程要慢。此外，蛋白激酶C激活剂佛波酯抑制血管紧张素II诱导的反应，但不抑制PDGF诱导的反应。这些结果表明，PDGF在VSMC中诱导磷脂酶C反应，但提示PDGF作用于磷脂酶C的信号传导机制与血管紧张素II不同。
