Kariya K I, Kawahara Y, Tsuda T, Fukuzaki H, Takai Y
Atherosclerosis. 1987 Feb;63(2-3):251-5. doi: 10.1016/0021-9150(87)90128-6.
In cultured rabbit aortic vascular smooth muscle cells (VSMC), protein kinase C-activating phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12,13-dibutyrate (PDBu) stimulated DNA synthesis in the presence of 10% cell-free plasma-derived serum. This stimulation was half that shown by PDGF. 4 alpha-Phorbol-12,13-didecanoate, known to be inactive for protein kinase C, was without effect in stimulating DNA synthesis. Prolonged treatment of the cells with PDBu led to a marked decrease in protein kinase C. In the pDBu-treated cells, the TPA-stimulated DNA synthesis was completely abolished whereas the PDGF-stimulated DNA synthesis was decreased to about half that in the control cells. These results suggest that protein kinase C is involved in PDGF-stimulated proliferation of VSMC.
在培养的兔主动脉血管平滑肌细胞(VSMC)中,蛋白激酶C激活剂佛波酯,如12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)和佛波醇 - 12,13 - 二丁酸酯(PDBu),在含有10%无细胞血浆源性血清的情况下刺激DNA合成。这种刺激作用是血小板衍生生长因子(PDGF)的一半。已知对蛋白激酶C无活性的4α - 佛波醇 - 12,13 - 二癸酸酯在刺激DNA合成方面没有作用。用PDBu对细胞进行长时间处理导致蛋白激酶C显著减少。在经PDBu处理的细胞中,TPA刺激的DNA合成完全被消除,而PDGF刺激的DNA合成减少至对照细胞的约一半。这些结果表明蛋白激酶C参与了PDGF刺激的VSMC增殖。