Differences in steroidogenic acute regulatory protein expression from the luteinizing-granulosa cells of patients undergoing in vitro fertilization with embryo transfer: Implications for cycle outcomes

Abstract

Objective: Previous research has suggested a correlation between the subtle rise in progesterone induced by the administration of human chorionic gonadotropin (hCG) and cycle outcome in patients undergoing in vitro fertilization with embryo transfer (IVF-ET). The data suggest that patients who have <2-fold increase in progesterone levels will not conceive as a result of that IVF-ET attempt (poor responders). Further, if the luteinizing-granulosa cells of poor responders are placed in culture, their steroid hormone production will be significantly less than that of the luteinizing-granulosa cells of patients with a normal response to hCG (>3-fold; normal responders). Recent studies have demonstrated that steroidogenic acute regulatory protein (StAR) regulates the rate-limiting step in steroid hormone biosynthesis. The objective of the present study was to determine whether StAR expression differed in normal responders and poor responders undergoing IVF-ET. Study Design: The luteinizing-granulosa cells of 6 patients were isolated after follicular aspiration and assayed for StAR expression. Three sets of cells were from patients exhibiting a normal response to hCG administration and 3 sets were from patients exhibiting a poor response. Results: Data suggest a 17% drop in StAR protein in patients with a poor response to hCG administration when compared with those with a normal response. Conclusions: Although StAR protein was expressed in all 6 cellular extracts, expression appeared greatest in cells recovered from normal responders. Further, although two thirds of the patients with a normal response reported term pregnancies, no pregnancies were reported in the poor responders. Low levels of progesterone and absence of pregnancy may be due to a defect in the mechanism that converts granulosa and theca-lutein cells to luteal cells after the luteinizing hormone surge (or hCG administration). Data from the current study would suggest that the StAR protein may be involved. (Am J Obstet Gynecol 2002;186:872-5.)