Neichi T, Chang W C, Mitsui Y, Murota S
Artery. 1982;11(1):47-63.
Prostaglandin biosynthetic activity of miniature-pig aortic endothelial cells was compared with that of smooth muscle cells in culture. When used as homogenates, endothelial cells produced mainly PGE2 and 6-ketoPGF1 alpha (degradated product of PGI2) from arachidonic acid, while they produced a large amount of PGF2 alpha in addition to these when used as intact cells. Intact smooth muscle cells and their homogenates produced PGE2 as a major product. 6-KetoPGF1 alpha was produced by smooth muscle cells in the first few generations and became undetectable after several cultivations. 6-KetoPGF1 alpha and PGE2 were produced by intact or endothelium-depleted aortas. Our results suggest that both endothelial cells and smooth muscle cells in porcine aorta possess PGI2 and PGE2 biosynthetic activities. The subcultivation of smooth muscle cells, but not endothelial cells, in vitro resulted in the rapid disappearance of PGI2 synthetase activity. The PGI2 biosynthetic activity of endothelial cells was several fold higher than that of smooth muscle cells. Porcine smooth muscle cells' low ability to produce PGI2 may offer a reason why atherosclerosis is easily developed in pigs.
将培养的小型猪主动脉内皮细胞与平滑肌细胞的前列腺素生物合成活性进行了比较。当用作匀浆时,内皮细胞主要从花生四烯酸产生PGE2和6-酮-PGF1α(PGI2的降解产物),而当用作完整细胞时,除了这些之外,它们还产生大量的PGF2α。完整的平滑肌细胞及其匀浆以PGE2作为主要产物。6-酮-PGF1α在前几代平滑肌细胞中产生,经过几次传代培养后变得无法检测到。完整的或去除内皮的主动脉可产生6-酮-PGF1α和PGE2。我们的结果表明,猪主动脉中的内皮细胞和平滑肌细胞都具有PGI2和PGE2生物合成活性。体外平滑肌细胞(而非内皮细胞)的传代培养导致PGI2合成酶活性迅速消失。内皮细胞的PGI2生物合成活性比平滑肌细胞高几倍。猪平滑肌细胞产生PGI2的能力较低,这可能是猪易患动脉粥样硬化的一个原因。