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Endocrinology, Vol 136, 1388-1393, Copyright © 1995 by Endocrine Society
ARTICLES |
M Yamaguchi, T Imai, T Maeda, M Sakata and A Miyake
Department of Obstetrics and Gynecology, Osaka University Medical School, Japan.
To determine whether cAMP regulates mouse placental lactogen-I (mPL-I) and mPL-II secretion at midpregnancy in vitro, mouse placental tissue from day 9 of pregnancy was dispersed with collagenase, cells were fractionated on a Percoll gradient, and the purified trophoblast cells were plated in a serum-free medium. The cells were then incubated with various agents that increased the intracellular cAMP level for 5 days. 8-Bromo-cAMP stimulated mPL-I secretion, but inhibited mPL-II secretion in a time- and dose-dependent manner without changing the amount of newly synthesized trichloroacetic acid-precipitable proteins. Cholera toxin and forskolin, which increase intracellular cAMP accumulation, also regulated mPL-I and mPL-II secretion in the same manner. 8-Bromo- cAMP increased the intracellular mPL-I concentration, decreased the intracellular mPL-II concentration, and increased the immunoprecipitable newly synthesized mPL-I concentration in both the medium and cells. 8-Bromo-cAMP increased the expression of mPL-I messenger RNA and decreased the expression of mPL-II messenger RNA. The sequential reverse hemolytic plaque assay and double immunocytochemistry indicated that 8-bromo-cAMP regulates the subpopulation of giant cells containing and releasing mPL. These findings suggest that an increase in intracellular cAMP stimulates mPL- I secretion, but inhibits mPL-II secretion by changing the subpopulation of giant cells containing and releasing mPL.
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