Morisaki N, Kanzaki T, Motoyama N, Saito Y, Yoshida S
Second Department of Internal Medicine, School of Medicine, Chiba University, Japan.
Atherosclerosis. 1988 Jun;71(2-3):165-71. doi: 10.1016/0021-9150(88)90140-2.
The role of prostaglandin I2 (PGI2) in the control of DNA synthesis during the cell cycle was investigated in cultured rabbit aortic smooth muscle cells (SMC). SMC at confluency in the G0 state reached the S phase about 16 h after stimulation with serum, as judged by measurement of [3H]thymidine incorporation into DNA (DNA synthesis). Cyclooxygenase inhibitors such as indomethacin and aspirin enhanced DNA synthesis, suggesting that endogenously synthesized prostaglandins inhibit DNA synthesis. Added PGE1 or PGE2 had little effect on DNA synthesis. PGI2 inhibited DNA synthesis only when added from 10 to 16 h after stimulation of SMC in the G0 state with serum. Addition of CS-570, a stable PGI2 analogue, inhibited DNA synthesis at any time after serum stimulation. The endogenous syntheses of PGI2 and DNA were negatively correlated. These results suggest that PGI2 inhibits DNA synthesis by acting on the progression stage of the G1 state.
在培养的兔主动脉平滑肌细胞(SMC)中研究了前列腺素I2(PGI2)在细胞周期中对DNA合成的调控作用。处于G0期的汇合SMC在用血清刺激后约16小时进入S期,这通过测量[3H]胸苷掺入DNA(DNA合成)来判断。吲哚美辛和阿司匹林等环氧化酶抑制剂可增强DNA合成,表明内源性合成的前列腺素会抑制DNA合成。添加PGE1或PGE2对DNA合成影响不大。仅在处于G0期的SMC用血清刺激后10至16小时添加PGI2时,它才会抑制DNA合成。添加稳定的PGI2类似物CS-570在血清刺激后的任何时间都会抑制DNA合成。PGI2的内源性合成与DNA呈负相关。这些结果表明,PGI2通过作用于G1期的进展阶段来抑制DNA合成。