Abstract
The luteinizing hormone/chorionic gonadotropin receptor (LHCGR) is essential for fertility in men and women. LHCGR binds luteinizing hormone (LH) as well as the highly homologous chorionic gonadotropin. Signaling from LHCGR is required for steroidogenesis and gametogenesis in males and females and for sexual differentiation in the male. The importance of LHCGR in reproductive physiology is underscored by the large number of naturally occurring inactivating and activating mutations in the receptor that result in reproductive disorders. Consequently, several genetically modified mouse models have been developed for the study of LHCGR function. They include targeted deletion of LH and LHCGR that mimic inactivating mutations in hormone and receptor, expression of a constitutively active mutant in LHCGR that mimics activating mutations associated with familial male-limited precocious puberty and transgenic models of LH and hCG overexpression. This review summarizes the salient findings from these models and their utility in understanding the physiological and pathological consequences of loss and gain of function in LHCGR signaling.
Highlights
The luteinizing hormone/chorionic gonadotropin receptor (LHCGR), together with the glycoprotein hormone receptors, follicle-stimulating hormone receptor (FSHR) and thyroid stimulating hormone receptor (TSHR), belongs to the G protein-coupled receptor superfamily [1]
Female KO mice were phenotypically normal at birth, which is not surprising since female sexual differentiation is independent of ovarian function and ovarian LHCGR expression begins after birth [57, 58]
This study showed that progression of folliculogenesis beyond the antral stage and induction of ovulation could not be achieved by hCG or recombinant FSH in the absence of LHCGR
Summary
Reviewed by: Emma June Petrie, The Walter and Eliza Hall Institute of Medical Research, Australia Chengcheng “Alec” Zhang, University of Texas Southwestern Medical Center, USA
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