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Changes in Insulin-like Growth Factor-Binding Protein-3 Messenger Ribonucleic Acid in Endothelial Cells of the Human Corpus Luteum: A Possible Role in Luteal Development and Rescue

Medical Research Council Reproductive Biology Unit (H.M.F., S.F.L., W.C.D., F.E.R., P.J.I.), Center for Reproductive Biology, Edinburgh EH3 9ET, United Kingdom; and Department of Reproductive Medicine (H.K., G.F.E.), University of California at San Diego, La Jolla, California 92093-0674

Address correspondence and requests for reprints to: Dr. H. M. Fraser, Medical Research Council Reproductive Biology Unit, Centre for Reproductive Biology, 37 Chalmers Street, Edinburgh EH3 9ET, United Kingdom. E-mail: h.fraser{at}ed-rbu.mrc.ac.uk

In the human menstrual cycle, extensive angiogenesis accompanies luteinization; and the process is physiologically important for corpus luteum (CL) function. During luteolysis, the vasculature collapses, and the endothelial cells die. In a conceptual cycle, the CL persists both functionally and structurally beyond the luteoplacental shift. Although luteal rescue is not associated with increased angiogenesis, endothelial survival is extended. Despite the central role of the luteal vasculature in fertility, the mechanisms regulating its development and demise are poorly understood. There is increasing evidence that insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) may be important effectors of luteal function. Here, we have found that IGFBP-3 messenger RNA is expressed in the endothelium of the human CL and that the levels of message change during luteal development and rescue by human CG. The signal was strong during the early luteal phase, but it showed significant reduction during the mid- and late luteal phases. Interestingly, administration of human CG caused a marked increase in the levels of IGFBP-3 messenger RNA in luteal endothelial cells that was comparable to that observed during the early luteal phase. We conclude that endothelial cell IGFBP-3 expression is a physiological property of the CL of menstruation and pregnancy. These observations raise the intriguing possibility that the regulated expression of endothelial IGFBP-3 may play a role in controlling angiogenesis and cell responses in the human CL by autocrine/paracrine mechanisms.

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