Induced luteal regression: differential effects on follicular and luteal inhibin/activin subunit mRNAs in the marmoset monkey.
During the luteal phase of the primate ovulatory cycle the predominant inhibin/activin subunit mRNAs produced by the corpus luteum and antral follicles are those for the alpha- and beta B-subunits respectively. The control of expression of these mRNAs and the resultant nature of the endocrine and paracrine signals which they may potentially generate has yet to be elucidated. Inhibin/activin subunit mRNAs may have a role in both the paracrine regulation of follicular and luteal function and modulation of FSH secretion. The aim of this study was to investigate the expression of inhibin/activin subunit mRNAs following luteal regression induced by either withdrawal of LH support (GnRH antagonist treatment), or by a direct inhibitory action (prostaglandin administration). Marmoset monkeys with regular ovulatory cycles were treated on day 8 and 9 of the luteal phase with either GnRH antagonist, prostaglandin or vehicle (n = 3 per group). Ovaries were studied 48 h after onset of treatment (on day 10 of the luteal phase) by hybridizing frozen tissue sections with radiolabelled riboprobes specific to the inhibin/activin alpha-, beta A- and beta B-subunit mRNAs. After autoradiographic exposure, grain concentrations were quantified by image analysis. In corpora lutea from control marmosets there was high expression of alpha-mRNA with only marginal expression of beta B-mRNA. Corpora lutea in animals treated with GnRH antagonist or prostaglandin had markedly reduced expression of alpha-mRNA while beta B-mRNA was unchanged. In controls, all healthy antral follicles exhibited a high level of expression of beta B-mRNA in the granulosa cells and low expression of alpha-mRNA in theca cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Fraser
H M
HM
MRC Reproductive Biology Unit, University of Edinburgh, UK.
Lunn
S F
SF
Whitelaw
P F
PF
Hillier
S G
SG
D028341:Activins; D000818:Animals; D001345:Autoradiography; D002144:Callithrix; D003338:Corpus Luteum / Q000378:metabolism*; D015237:Dinoprost / Q000494:pharmacology; D005260:Female; D015870:Gene Expression; D007987:Gonadotropin-Releasing Hormone / Q000037:antagonists & inhibitors; D007091:Image Processing, Computer-Assisted; D017403:In Situ Hybridization; D007265:Inhibins / Q000235:genetics / Q000378:metabolism*; D003341:Luteolysis / Q000502:physiology*; D009842:Oligopeptides / Q000494:pharmacology; D006080:Ovarian Follicle / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism*
D009842:Oligopeptides; D012333:RNA, Messenger; D028341:Activins; D007987:Gonadotropin-Releasing Hormone; D007265:Inhibins; C057022:iturelix; D015237:Dinoprost