Agents that increase cellular cyclic AMP inhibit proliferative activity and decrease lipid content in cells cultured from atherosclerotic human aorta.
Cholera toxin, methylisobutylxanthine and prostacyclin (PGI2) analogues as well as dibutyryl cyclic AMP inhibit by 2-7-fold 3H-thymidine uptake into intimal cells isolated from atherosclerotic human aorta in primary culture. These agents also decrease cholesteryl ester and triglyceride levels and do not affect content of phospholipids and free cholesterol in cells cultured from atherosclerotic lesions.
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology*; D001011:Aorta / Q000378:metabolism*; D001161:Arteriosclerosis / Q000378:metabolism*; D003994:Bucladesine / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D002772:Cholera Toxin / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism*; D011464:Epoprostenol / Q000494:pharmacology* / Q000031:analogs & derivatives; D006801:Humans; D066298:In Vitro Techniques; D008055:Lipids / Q000032:analysis; D013806:Theophylline / Q000031:analogs & derivatives*; D013936:Thymidine / Q000378:metabolism
D008055:Lipids; D003994:Bucladesine; C026678:carboprostacyclin; D002772:Cholera Toxin; D013806:Theophylline; D011464:Epoprostenol; D000242:Cyclic AMP; D015056:1-Methyl-3-isobutylxanthine; D013936:Thymidine