Mindy S Christianson1, Melissa Yates. 1. Division of Reproductive Endocrinology and Infertility, Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Lutherville, Maryland 20193, USA.
Abstract
PURPOSE OF REVIEW: Multiple studies have demonstrated a role for scavenger receptor class B type 1 (SR-B1) in female fertility. Recent studies have implicated specific SR-B1 gene polymorphisms in decreased progesterone production and suboptimal fertility outcomes. RECENT FINDINGS: The lipoprotein receptor SR-B1 has been known to mediate selective uptake of lipids into steroidogenic tissues such as the ovaries. SR-B1 plays a major role in the ability of the corpus luteum to produce progesterone, which is known to play a key role in sustaining early pregnancy. Animal studies have demonstrated that deficiency in SR-B1 results in subfertility that can be restored with addition of SR-B1 function. Single-nucleotide polymorphisms in SCARB1, the gene encoding SR-B1, have been associated with human lipid levels. Women undergoing infertility treatment with low SR-B1 expression in granulosa cells were noted to have plasma estradiol levels half the normal levels and a significantly lower number of retrieved oocytes. In vitro, deficiency of SR-B1 is associated with lower progesterone secretion in human granulosa cells. Certain SR-B1 polymorphisms have been associated with lower follicular progesterone levels and a significantly lower clinical pregnancy rate. SUMMARY: Deficiency of SR-B1, particularly due to single-nucleotide polymorphisms, could explain some features of female human infertility.
PURPOSE OF REVIEW: Multiple studies have demonstrated a role for scavenger receptor class B type 1 (SR-B1) in female fertility. Recent studies have implicated specific SR-B1 gene polymorphisms in decreased progesterone production and suboptimal fertility outcomes. RECENT FINDINGS: The lipoprotein receptor SR-B1 has been known to mediate selective uptake of lipids into steroidogenic tissues such as the ovaries. SR-B1 plays a major role in the ability of the corpus luteum to produce progesterone, which is known to play a key role in sustaining early pregnancy. Animal studies have demonstrated that deficiency in SR-B1 results in subfertility that can be restored with addition of SR-B1 function. Single-nucleotide polymorphisms in SCARB1, the gene encoding SR-B1, have been associated with humanlipid levels. Women undergoing infertility treatment with low SR-B1 expression in granulosa cells were noted to have plasma estradiol levels half the normal levels and a significantly lower number of retrieved oocytes. In vitro, deficiency of SR-B1 is associated with lower progesterone secretion in human granulosa cells. Certain SR-B1 polymorphisms have been associated with lower follicular progesterone levels and a significantly lower clinical pregnancy rate. SUMMARY:Deficiency of SR-B1, particularly due to single-nucleotide polymorphisms, could explain some features of female humaninfertility.
Authors: Joseph U Igietseme; Yusuf Omosun; Olga Stuchlik; Matthew S Reed; James Partin; Qing He; Kahaliah Joseph; Debra Ellerson; Brigid Bollweg; Zenas George; Francis O Eko; Claudiu Bandea; Hsi Liu; Genyan Yang; Wun-Ju Shieh; Jan Pohl; Kevin Karem; Carolyn M Black Journal: PLoS One Date: 2015-12-17 Impact factor: 3.240