Estradiol stimulation of inositolphospholipid metabolism in human endometrial fibroblasts.
Stimulated inositolphospholipid turnover has been proposed to constitute a signal-transducing mechanism in many cell types. To determine the inositolphospholipid turnover during stimulation by 17 beta-estradiol, the turnover kinetics of phospholipids was investigated in human endometrial fibroblasts. In cells incubated with [32P] phosphate for 1 h, estradiol rapidly and persisitently (for at least 30 min) enhanced the rate of 32P-labeling of phosphatidic acid (PA). On the other hand, after a lag time of 5 min, 32P-labeling of phosphatidylinositol (PI) was also increased also. These sequential 32P-labeling of PA and PI demonstrated that inositolphospholipid turnover was stimulated in fibroblasts exposed to estradiol. The rapid estrogen-stimulated inositolphospholipid turnover may not be through the mechanism associated with classical action of estrogen.
Iida
K
K
Department of Obstetrics and Gynecology, Gifu University School of Medicine, Japan.
Imai
A
A
Tamaya
T
T
D004717:Endometrium / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D007295:Inositol Phosphates / Q000378:metabolism*; D010712:Phosphatidic Acids / Q000378:metabolism; D010716:Phosphatidylinositols / Q000378:metabolism; D010761:Phosphorus Radioisotopes
D007295:Inositol Phosphates; D010712:Phosphatidic Acids; D010716:Phosphatidylinositols; D010761:Phosphorus Radioisotopes; D004958:Estradiol