Insulin-like growth factor binding protein-3 mRNA expression in endothelial cells of the primate corpus luteum.
Luteinization is associated with endothelial cell proliferation as part of the extensive angiogenesis necessary to maintain corpus luteum function. However, following luteal demise, the vasculature regresses and the endothelial cells disappear. In the rat corpus luteum, the endothelial cells express high concentrations of insulin-like growth factor-binding protein-3 (IGFBP-3) during luteolysis, suggesting a role of IGFBP-3 during endothelial cell loss. The aim of the present study was to determine the occurrence and location of the messenger ribonucleic acid (mRNA) for IGFBP-3 in the primate corpus luteum, and to determine whether or not induction of luteal regression is associated with changes in localization of the message. Marmoset corpora lutea were studied throughout the cycle. The effects of induced luteolysis were examined 12 h or 24 h after treatment with either a gonadotrophin-releasing hormone antagonist or a prostaglandin F2alpha analogue, administered during the mid-luteal phase. High IGFBP-3 expression was recorded in the endothelial cells of the majority of microvessels and a minority of capillaries surrounding the lutein cells in all functionally active corpora lutea. Expression declined markedly in regressing corpora lutea of the late follicular phase. Expression of the IGFBP-3 mRNA in lutein cells in the control corpus luteum was extremely rare. There were no major differences in the degree and pattern of IGFBP-3 expression as a consequence of induced luteal regression although there was an apparent increase in the number of capillary endothelial cells expressing. Induction of luteolysis resulted in expression in a minority of lutein cells. These results support the concept that IGFBP-3 has an autocrine/paracrine role in regulating various cell types in the primate corpus luteum, including endothelial cells. However, expression of IGFBP-3 mRNA throughout the luteal phase suggests it may regulate angiogenesis and luteal function rather than endothelial cell death and luteolysis.
Fraser
H M
HM
MRC Reproductive Biology Unit, Edinburgh, UK.
Lunn
S F
SF
Kim
H
H
Erickson
G F
GF
D000818:Animals; D002144:Callithrix; D002196:Capillaries / Q000166:cytology / Q000378:metabolism; D003338:Corpus Luteum / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D007987:Gonadotropin-Releasing Hormone / Q000037:antagonists & inhibitors; D006727:Hormone Antagonists / Q000494:pharmacology; D017403:In Situ Hybridization; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000235:genetics*; D003341:Luteolysis / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D009842:Oligopeptides / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics* / Q000378:metabolism*; D051381:Rats
D006727:Hormone Antagonists; D018972:Insulin-Like Growth Factor Binding Protein 3; D009842:Oligopeptides; D012333:RNA, Messenger; D007987:Gonadotropin-Releasing Hormone; D015237:Dinoprost; C084350:antarelix