Disease relevance of Lhcgr

• Genetic heterogeneity of constitutively activating mutations of the human luteinizing hormone receptor in familial male-limited precocious puberty [1].
• These findings support the hypothesis that high natural resistance to leishmaniasis (Lshr) is expressed as a microbistatic effect, exerted within the parasitized macrophage of the host [2].

High impact information on Lhcgr

• Fertility in luteinizing hormone receptor-knockout mice after wild-type ovary transplantation demonstrates redundancy of extragonadal luteinizing hormone action [3].
• The luteinizing hormone receptor (LHR), mainly expressed in gonads, is essential for normal reproduction [3].
• Hsf2(-/-) females also display hormone response defects, that can be rescued by superovulation treatment, and exhibit abnormal rates of luteinizing hormone receptor mRNAs [4].
• The persistent follicle-stimulating hormone action in luteinizing hormone receptor knockout mice apparently stimulates spermatogenesis up to postmeiotic round spermatids, as observed in gonadotropin-deficient rodent models on follicle-stimulating hormone supplementation [5].
• In vitro, but not in vivo, AMH also decreases the expression of the luteinizing hormone receptor [6].

Biological context of Lhcgr

• In conclusion, deletion and reinsertion of Lhcgr further support that uterine Cox2 gene expression is dependent on LH signaling [7].
• Normal prenatal but arrested postnatal sexual development of luteinizing hormone receptor knockout (LuRKO) mice [8].
• Knockout of luteinizing hormone receptor abolishes the effects of follicle-stimulating hormone on preovulatory maturation and ovulation of mouse graafian follicles [9].
• Luteinizing hormone receptor knockout (LuRKO) mice and transgenic human chorionic gonadotropin (hCG)-overexpressing mice (hCG alphabeta+) have bone phenotypes [10].
• Finally, two 5'-flanking sequences ( approximately 2 and 4 kb) of the rat LHR gene were shown to direct expression of the lacZ reporter to specific areas of the peripheral and central nervous system in fetal and adult transgenic mice, especially to structures associated with sensory, memory, reproductive behavior, and autonomic functions [11].

Anatomical context of Lhcgr

• Using a clonal cell line that stably expresses the murine luteinizing hormone receptor (LHR 11/6 cells), we studied the molecular mechanisms of agonist-induced desensitization of the luteinizing hormone/chorionic gonadotropin-responsive adenylyl cyclase [12].
• Transgenic mice harboring murine luteinizing hormone receptor promoter/beta-galactosidase fusion genes: different structural and hormonal requirements of expression in the testis, ovary, and adrenal gland [13].
• Assessment of mechanisms of thyroid hormone action in mouse Leydig cells: regulation of the steroidogenic acute regulatory protein, steroidogenesis, and luteinizing hormone receptor function [14].
• The objective of this study was to assess the mechanism by which oocytes suppress FSH-induced LHR expression [15].
• However, oocytes dramatically suppressed 8Br-cAMP-induced LHR mRNA steady-state expression by granulosa cells [15].

Associations of Lhcgr with chemical compounds

• The Lhcgr knockout (herein designated LHRKO) animals have implantation failure even after estradiol and progesterone therapy [7].
• Testosterone replacement therapy induces spermatogenesis and partially restores fertility in luteinizing hormone receptor knockout mice [16].
• Progesterone can participate in down-regulation of the luteinizing hormone receptor gene expression and function in cultured murine Leydig cells [17].
• Luteinizing hormone (LH) and chorionic gonadotropin (CG) are heterodimeric glycoprotein hormones acting on the luteinizing hormone receptor (LHR) [18].
• RESULTS: Expression of the transgene correlated with three Lshr-associated lipopolysaccharide/interferon-gamma-regulated macrophage activation phenotypes: respiratory burst, nitrite release, and uptake of L-arginine [19].

Other interactions of Lhcgr

• Regulation of luteinizing hormone-receptor and follicle-stimulating hormone-receptor messenger ribonucleic acid levels during development in the neonatal mouse ovary [20].
• Luteinizing hormone receptor-mediated effects on initiation of spermatogenesis in gonadotropin-deficient (hpg) mice are replicated by testosterone [21].
• In addition, the effect of oocytes on 8Br-cAMP-induced LHR mRNA steady-state expression by granulosa cells was assessed by RNase protection assays [15].
• Regulation of luteinizing hormone receptor gene expression by insulin-like growth factor-I in an immortalized murine Leydig tumor cell line (BLT-1) [22].

Analytical, diagnostic and therapeutic context of Lhcgr

• After calibration in a mouse Leydig cell bioassay against the WHO LH80/522 standard, the ED (50) of the CG preparation on a COS7 cell line permanently expressing the marmoset LHR was 4.25 +/- 0.21 IU/L (n = 3) [18].
• Use of tritiated thymidine incorporation and autoradiography to label dividing amastigotes showed equivalent multiplication of the parasite in liver macrophages from Lshs and Lshr mice between 24 h and 48 h after infection in vitro, with a dramatic difference observed thereafter [23].

References