Differential control of immunoreactive alpha-inhibin and progesterone production by marmoset luteal cells in vitro: evidence for a paracrine action of alpha-inhibin on basal and gonadotropin-stimulated progesterone production.
There is an increase in plasma concentrations of immunoreactive (ir) inhibin unaccompanied by a rise in plasma progesterone during early pregnancy in the marmoset monkey. We investigated the potential involvement of hCG and prostaglandin E2 (PGE2) in stimulating a selective increase in inhibin concentrations by measuring the production of ir-alpha-inhibin and progesterone by dispersed luteal cells cultured under serum-free conditions. After one day, hCG had no effect on progesterone production by the cells but stimulated a significant increase (p < 0.05) in alpha-inhibin production. PGE2 significantly increased progesterone production (p < 0.001) but inhibited the production of alpha-inhibin (p < 0.001). After three days of culture, output of alpha-inhibin fell to low levels and no significant effect of hCG or PGE2 was detected. Progesterone also fell with time in culture, but hCG maintained production resulting in a significant increase above control levels (p < 0.001). The addition of low density lipoproteins (LDL) to the culture medium increased progesterone production (p < 0.001) while decreasing alpha-inhibin production (p < 0.01). Immunoneutralization of endogenous alpha-inhibin resulted in a significant decrease in both basal (p < 0.05) and gonadotropin-stimulated (p < 0.05) progesterone concentrations. These results provide further evidence for differential control of progesterone and alpha-inhibin production by marmoset luteal cells and show that hCG can selectively stimulate alpha-inhibin production. In addition, alpha-inhibin may have a local paracrine action in the marmoset CL, enhancing both basal and gonadotropin-stimulated progesterone secretion.
Webley
G E
GE
MRC/AFRC Comparative Physiology Group, Institute of Zoology, Regent's Park, London, United Kingdom.
Marsden
P L
PL
Knight
P G
PG
D000818:Animals; D002144:Callithrix; D002478:Cells, Cultured; D006063:Chorionic Gonadotropin / Q000494:pharmacology*; D003470:Culture Media; D015232:Dinoprostone / Q000494:pharmacology; D004815:Epidermal Growth Factor / Q000494:pharmacology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000494:pharmacology; D007265:Inhibins / Q000494:pharmacology*; D008077:Lipoproteins, LDL / Q000494:pharmacology; D008184:Luteal Cells / Q000187:drug effects / Q000378:metabolism*; D011374:Progesterone / Q000096:biosynthesis* / Q000097:blood; D013997:Time Factors
D006063:Chorionic Gonadotropin; D003470:Culture Media; D008077:Lipoproteins, LDL; D011374:Progesterone; D007265:Inhibins; D004815:Epidermal Growth Factor; D005640:Follicle Stimulating Hormone; D015232:Dinoprostone