Luteotropic effects of follicle-stimulating hormone (FSH): II. FSH luteinizing hormone, and prolactin effects on second messenger systems in the corpus luteum of the pregnant hamster.
We have recently shown that FSH, LH, and prolactin (PRL)--alone or combined--act as luteotropins when incubated with luteal cells from pregnant hamsters (Yuan and Greenwald, Biol Reprod 1994; 51:43-49). The purpose of the present study was to determine which second messenger systems are affected by these hormones with progesterone (P4) synthesis as the principal endpoint after 4 h of incubation with 100,000 luteal cells. Luteal cells on Days 4, 10, or 12 of pregnancy were incubated with the following reagents: 10 ng of recombinant human FSH (r-hFSH), ovine (o) FSH, oLH, oPRL, forskolin, db-cAMP, protein kinase A inhibitor (PKI), protein kinase C activator (phorbol 12-myristate 13-acetate; PMA), or various combinations of the reagents. Forskolin and db-cAMP each stimulated P4 in a dose-dependent manner, while PKI significantly inhibited forskolin-, r-hFSH-, oFSH-, and oLH-stimulated P4 on Day 4 of pregnancy. PMA (0.001-1.0 microM) did not affect basal P4 on Day 4, 10, or 12 of pregnancy; however, 100 nM PMA inhibited db-cAMP-, forskolin-, oFSH-, and oLH-stimulated P4 synthesis on Days 4 and 12. The antagonistic effects of PMA were reversed in all cases by concurrent incubation with a PKC inhibitor, H-7. On Day 4 of pregnancy, P4 was stimulated by oFSH and oLH with the highest levels observed in medium stimulated by the luteotropic complex of oFSH, oLH, and oPRL. Recombinant hFSH enhanced P4 production in a dose-dependent manner; doses of 10 ng and above resulted in statistically significant differences from the control values (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Yuan
W
W
Department of Physiology, Ralph L. Smith Research Center, University of Kansas Medical Center, Kansas City 66160-7401.
Greenwald
G S
GS
D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology; D003338:Corpus Luteum / Q000187:drug effects / Q000378:metabolism*; D006224:Cricetinae; D000242:Cyclic AMP / Q000096:biosynthesis; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors; D004789:Enzyme Activation / Q000187:drug effects; D005260:Female; D005640:Follicle Stimulating Hormone / Q000494:pharmacology*; D007986:Luteinizing Hormone / Q000494:pharmacology*; D011247:Pregnancy; D011374:Progesterone / Q000096:biosynthesis; D011388:Prolactin / Q000494:pharmacology*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism; D011994:Recombinant Proteins / Q000494:pharmacology; D015290:Second Messenger Systems / Q000187:drug effects*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D011994:Recombinant Proteins; D005576:Colforsin; D011374:Progesterone; D003994:Bucladesine; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate