Triiodothyronine stimulates prostacyclin production by rat aortic smooth muscle cells in culture.
The effect of triiodothyronine (T3) on prostacyclin production in rat aortic smooth muscle cells was investigated by using an intact cell assay system. T3 at its physiological concentrations has no significant effect on smooth muscle cell proliferation, but it does significantly stimulate prostacyclin production by the cells. Maximum stimulation of prostacyclin production is obtained when cells are treated with T3 for 4 consecutive days. The dose--response curve shows a linear relationship between the stimulation of prostacyclin production and T3 concentrations in the range 0.007--10 microgram/dl. The maximal prostacyclin production by T3-treated cells (at a concentration of 10 microgram/dl), is 270% compared with control cells. T3 treatment shows no significant effect on phospholipase (and/or lipase) activities. Our results suggest that thyroid hormone might play an important physiological role in the protection of arteries from atherosclerotic changes by stimulating prostacyclin production in arterial smooth muscle cells.
D000818:Animals; D001011:Aorta / Q000378:metabolism; D001095:Arachidonic Acids / Q000378:metabolism; D001161:Arteriosclerosis / Q000209:etiology; D004305:Dose-Response Relationship, Drug; D011464:Epoprostenol / Q000096:biosynthesis*; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats; D014284:Triiodothyronine / Q000494:pharmacology*
D001095:Arachidonic Acids; D011453:Prostaglandins; D014284:Triiodothyronine; D011464:Epoprostenol