INSULIN-LIKE-GROWTH-FACTOR BINDING PROTEIN-3 MESSENGER-RNA EXPRESSIONIN ENDOTHELIAL-CELLS OF THE PRIMATE CORPUS-LUTEUM

Luteinization is associated with endothelial cell proliferation as par t of the extensive angiogenesis necessary to maintain corpus luteum fu nction. However, following luteal demise, the vasculature regresses an d the endothelial cells disappear. In the rat corpus luteum, the endot helial cells express high concentrations of insulin-like growth factor -binding protein-3 (IGFBP-3) during luteolysis, suggesting a role of I GFBP-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 chan ges in localization of the message. Marmoset corpora lutea were studie d throughout the cycle, The effects of induced luteolysis were examine d 12 h or 24 h after treatment with either a gonadotrophin-releasing h ormone antagonist or a prostaglandin Flee analogue, administered durin g the mid-luteal phase. High IGFBP-3 expression was recorded in the en dothelial cells of the majority of microvessels and a minority of capi llaries surrounding the lutein cells in all functionally active corpor a lutea, Expression declined markedly in regressing corpora lutea of t he late follicular phase. Expression of the IGFBP-3 mRNA in lutein cel ls in the control corpus luteum was extremely rare. There were no majo r differences in the degree and pattern of IGFBP-3 expression as a con sequence of induced luteal regression although there was an apparent i ncrease in the number of capillary endothelial cells expressing. Induc tion of luteolysis resulted in expression in a minority of lutein cell s. These results support the concept that IGFBP-3 has an autocrine/par acrine role in regulating various cell types in the primate corpus lut eum, 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.