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-ketoPGF(1α) (degradated product of PGI2) from arachidonic acid, while they produced a large amount of PGF(2α) in addition to these when used as intact cells. Intact smooth muscle cells and their homogenates produced PGE2 as a major product. 6-KetoPGF(1α) was produced by smooth muscle cells in the first few generations and became undetectable after several cultivations. 6-KetoPGF(1α) 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.
|Number of pages
|Published - 1982
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine