Estrous Cycle-Related Changes of High Affinity Luteinizing Hormone/Human Chorionic Gonadotropin Binding Sites in the Rat Uterus

Bonnamy, Pierre-Jacques; Benhaïm, Annie; Leymarie, P.

doi:10.1210/endo-126-2-1264

Cited by 34 publications

(21 citation statements)

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“…After dioestrus, the expression level of Lhcgr dropped significantly back down to the pro-oestrus level of the next cycle. Our qRT-PCR results confirmed and extended findings in the mouse model reported by Bonnamy et al (1990), who observed a cyclic variation in LHCGR binding to radiolabelled hCG in the rat endometrium. The increased Lhcgr expression at the time of implantation provides further support for a possible role of LHCGR signalling at the maternal-fetal interface during embryo implantation in mice.…”

Section: Discussionsupporting

confidence: 90%

Evidence for cross-talk between the LH receptor and LH during implantation in mice

Gridelet

Tsampalas

Berndt

et al. 2013

Reprod. Fertil. Dev.

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Abstract. The present study investigated the first interaction that occurs between the blastocyst and endometrium during implantation. Given the ethical objections to studying implantation in humans, a mouse model was used to study the dialogue between luteinising hormone (LH) and luteinising hormone receptor (LHCGR). Several studies performed on LHCGR-knockout mice have generated controversy regarding the importance of the dialogue between LH and LHCGR during implantation. There has been no demonstration of a bioactive LH-like signal produced by the murine blastocyst. The first aim of the present study was to examine and quantify, using radioimmunoassay, the generation of a bioactive LH signal by the murine blastocyst. We went on to examine and quantify endometrial Lhcgr expression to validate the mouse model. Expression of LHCGR in mouse uteri was demonstrated using immunohistochemistry and western blot analysis. To quantify the expression of Lh in the mouse blastocyst and Lhcgr in the endometrium, reverse transcription-polymerase chain reaction (RT-PCR) and real-time quantitative (q) RT-PCR were performed. The results demonstrate that Lhcgr expression in BALB/c mouse endometrial epithelium is increased at the time of implantation and indicate that LHCGR may contribute to the implantation process. In support of this hypothesis, we identified a bioactive LH signal at the time of murine blastocyst implantation.

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Section: Discussionsupporting

confidence: 90%

Evidence for cross-talk between the LH receptor and LH during implantation in mice

Gridelet

Tsampalas

Berndt

et al. 2013

Reprod. Fertil. Dev.

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“…It has been reported that the rat uterus contains LHR with an affinity constant for hCG that is analogous to that of rat ovarian receptors as shown in a previous study (3). The binding characteristics of these receptors were found to be similar to those reported for other animals (1,2), and these receptors have a high-binding-affinity constant and low-binding capacity.…”

Section: Discussionsupporting

confidence: 78%

Downregulation of LH receptor mRNA in the rat uterus

et al. 2012

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Abstract. We detected luteinizing hormone receptor (LHR) mRNA in the immature rat uterus by northern blotting and downregulation of this receptor mRNA after pregnant mare serum gonadotropin (PMSG)-human chorionic gonadotropin (hCG) treatment. After administration of hCG, the mRNA levels in the rat uterus declined to an extremely low level from Days 1 to 3 and then rebounded and reached higher than pretreatment values at Day 4. At Day 5 the levels were 3-fold higher than the control levels. The cultured uterus displayed an hCG concentration-dependent increase in cAMP production in the medium. Immunohistochemical experiments showed that these receptor proteins were expressed in the epithelial cells of the endometrium. These results suggest that functional LHRs are present in the immature rat uterus and are downregulated by signals resulting from hCG treatment. These data may support the idea that LH acts on the uterus to inhibit contraction at ovulation. Although the precise role of the LHR in the uterus remains unknown, this study may provide a model with which to investigate the regulation of LHR.

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“…Rao (1998) demonstrated that LH is able to induce cyclooxygenase 2 gene expression both in glandular epithelium and in stromal cells in human endometrium resulting in increased prostaglandin production (Zhoi et al 1997). The reported rise of uterine LHR/HCG receptor at metestrus in rats after ovulation (Bonnamy et al 1990) may be due to modulation of P 4 content (Bonnamy et al 1989). Our previous study also showed LH-induced increases in P 4 synthesis in mouse uterus at metestrus (Debnath et al 2000).…”

Section: Discussionmentioning

confidence: 66%

“…Contrary to this conventional belief, numerous studies demonstrated that the LH receptor (LHR)/HCG receptor is also present in a variety of non-gonadal tissues, particularly in the female reproductive tract (Bonnamy et al 1990, Reshef et al 1990, Lei et al 1993, Mukherjee et al 1994, Shemesh et al 1997, Ziecik et al 2005. Activation of this receptor in vivo and in vitro resulted in a wide variety of responses, which can be attributed to initiation and maintenance of pregnancy (Banaszak et al 2000, Srisuparp et al 2003, Lin et al 2005, Ziecik et al 2005.…”

Section: Introductionmentioning

confidence: 99%

Expression of LH receptor in nonpregnant mouse endometrium: LH induction of 3β-HSD and de novo synthesis of progesterone

Kundu

Pramanick

Paul

et al. 2012

Journal of Endocrinology

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In mouse uterus, at the late diestrus stage LH binding sites have previously been described. The aim of our study was to confirm the existence of LH receptor (Lhr (Lhcgr)) mRNA and its protein in mouse endometrium. Endometrium at all stages of the estrous cycle contained Lhr mRNA, essentially identical to that found in mouse ovary. Endometrium also contained a 72 kDa immunoreactive receptor protein that bound to mouse anti-LHR antibody in western blot. Both receptor mRNA and protein were maximally expressed in the endometrium at metestrus and LH caused a significant increase in their expression levels. Endometrium also contained 3b-hydroxy steroid dehydrogenase (3b-hsd) mRNA and 3b-HSD protein. LH addition elevated their expression and activity as evident from increased conversion of labeled pregnenolone to progesterone (P 4 ) and de novo P 4 synthesis. LH-induced endometrial P 4 synthesis is mediated through expression of steroidogenic acute regulatory (Star) gene. Results demonstrated that LH-induced P 4 synthesis in endometrium is possibly mediated through the cAMP pathway. Involvement of a MAPK pathway was also evident. Gonadotropin-stimulated endometrial P 4 synthesis was markedly attenuated by an antagonist of MEK1/2, PD98059. LH-stimulated MEK1/2-dependent phosphorylation of ERK1/2 in a concentration-and time-dependant manner in cultured endometrial tissues. Moreover, involvement of cAMP in LH-stimulated activation of ERK1/2 was also evident. It is therefore possible that the major signaling pathways regulating endometrial steroidogenesis in mouse, including the adenylate cyclase and MAP kinase pathways, converge at a point distal to activation of protein kinase A and ERK1/2.

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Estrous Cycle-Related Changes of High Affinity Luteinizing Hormone/Human Chorionic Gonadotropin Binding Sites in the Rat Uterus

Cited by 34 publications

References 0 publications

Evidence for cross-talk between the LH receptor and LH during implantation in mice

Evidence for cross-talk between the LH receptor and LH during implantation in mice

Downregulation of LH receptor mRNA in the rat uterus

Expression of LH receptor in nonpregnant mouse endometrium: LH induction of 3β-HSD and de novo synthesis of progesterone

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