Endocrinology, Vol 118, 244-249, Copyright © 1986 by Endocrine Society

ARTICLES

Hormonal control of phospholipid methylation in uterine luminal epithelial cells during uterine sensitivity to deciduogenic stimuli

BC Moulton and BB Koenig

Estrogen secretion during pregnancy or pseudopregnancy defines a period of uterine sensitivity to deciduogenic stimuli, perhaps by altering the capacity of the luminal epithelium to respond to these stimuli. In several types of cells, the transduction of signals acting upon cell membranes appears to involve activation of the transmethylation of membrane phospholipids. To examine the role of membrane phospholipid methylation in the development and loss of uterine sensitivity, the capacity of luminal epithelial cells to incorporate 3H-methyl groups from [methyl-3H]methionine into phospholipid was determined during pseudopregnancy and after progestin and estrogen treatment of ovariectomized rats to induce uterine sensitivity. During pseudopregnancy, phospholipid transmethylation increased between days 3 and 4 and then decreased. Phospholipid transmethylation also decreased after estradiol treatment of progestin-pretreated ovariectomized rats. Lowest levels of methylation were observed on day 6 of pseudopregnancy or after 36 h of estradiol treatment when the uterus was no longer sensitive to deciduogenic stimuli. One of the earliest uterine responses to deciduogenic stimuli is an increase in vascular permeability. When phospholipid methylation was inhibited in luminal epithelial cells by administration of 3-deazaadenosine, the increase in vascular permeability following a deciduogenic stimulus was inhibited. These data suggest that the primary responses of uterine luminal epithelial cells to deciduogenic stimuli may involve phospholipid methylation and that decreases in cellular capacity for phospholipid methylation result in decreases in uterine sensitivity to these stimuli.