Gonadotropin releasing hormone receptor gene and protein expression and immunohistochemical localization in bovine uterus and oviducts
ABSTRACT Recently GnRH, GnRH-R systems has been demonstrated in various extrahypothalamic and extrapituitary reproductive tissues in different mammalian species, where GnRH acts in an autocrine and or paracrine manner and modulates different biological processes. GnRH-R mRNA has also been demonstrated in bovine ovaries (follicle and corpus luteum) and normal and carcinogenic human endometrium/endometrial cells. This is the first study elucidating presence of GnRH-R mRNA and GnRH-R protein in bovine uterus and oviducts in follicular and luteal phases of the estrous cycle and further localizing the receptors to endometrial and oviductal epithelial cells. To our knowledge this is the first report demonstrating GnRH-R mRNA and protein in mammalian oviducts. We used gene-specific primers and monoclonal GnRH-R antibody to test GnRH-R mRNA and GnRH-R protein through RT-PCR and immunobloting. Immunohistochemistry was employed to localize these receptors to endometrial and oviductal epithelial cells. GnRH-R mRNA and receptor protein were expressed at expected molecular weights of 920bp and 60kD, respectively. Densitometry analysis revealed that expression levels for GnRH-R protein in uterus and oviducts were similar to bovine pituitary. The presence of GnRH receptors in bovine uterus and oviducts is intriguing and it would be imperative to examine the functional role of this system in the regulation of reproductive processes.
- SourceAvailable from: tdx.cat
- [Show abstract] [Hide abstract]
ABSTRACT: Establishment of the hypothalamic-hypophyseal-gonadal function is dependent on the highly controlled and dynamic interactions between regulatory signals from the brain, pituitary and gonads, all of them leading to the attainment of reproductive capacity, where a coordinated and timely activation of GnRH neurons must occur. The GnRH neurons extend their neurosecretory axons to the hypothalamus where GnRH is released into the pituitary portal vessels to elicit the secretion of LH and FSH, which in turn, will promote gonadal development and support reproductive physiology. Genetic studies have demonstrated that disabling mutations and targeted deletions of the G-protein-coupled receptor (GPR54) generated hypogonadotropic hypogonadism. This link between GPR54 and reproduction, generated attention to the natural ligands of the GPR54 receptor, known as kisspeptins, which are translational products of the hypothalamic gene KiSS1. Recent advances in kisspeptin research have defined a major role of this molecule in controlling the onset of the reproductive function observed at puberty. The aim of this review is to highlight the basic endocrine and genetic concepts involved in the establishment of the hypothalamic-hypophyseal-gonadal axis function which promotes the onset of the reproductive function during puberty. The review highlights what is currently known about the kisspeptin-GPR54 signalling system in the activation of the GnRH neurons.Journal of applied biomedicine 01/2010; 8(1):1-9. DOI:10.2478/v10136-009-0001-0 · 1.30 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: The hypothalamic-pituitary-gonadal (HPG) axis is the key reproductive regulator in vertebrates. While gonadotropin releasing hormone (GnRH), follicle stimulating (FSH), and luteinizing (LH) hormones are primarily produced in the hypothalamus and pituitary, they can be synthesized in the gonads, suggesting an intraovarian GnRH-gonadotropin axis. Because these hormones are critical for follicle maturation and steroidogenesis, we hypothesized that this intraovarian axis may be important in photoperiod-induced ovarian regression/recrudescence in seasonal breeders. Thus, we investigated GnRH-1 and gonadotropin mRNA and protein expression in Siberian hamster ovaries during (1) the estrous cycle; where ovaries from cycling long day hamsters (LD;16L:8D) were collected at proestrus, estrus, diestrus I, and diestrus II and (2) during photoperiod induced regression/recrudescence; where ovaries were collected from hamsters exposed to 14 weeks of LD, short days (SD;8L:16D), or 8 weeks post-transfer to LD after 14 weeks SD (PT). GnRH-1, LHβ, FSHβ, and common α subunit mRNA expression was observed in cycling ovaries. GnRH-1 expression peaked at diestrus I compared to other stages (p < 0.05). FSHβ and LHβ mRNA levels peaked at proestrus and diestrus I (p < 0.05), with no change in the α subunit across the cycle (p > 0.05). SD exposure decreased ovarian mass and plasma estradiol concentrations (p<0.05) and increased GnRH-1, LHβ, FSHβ, and α subunit mRNA expression as compared to LD and, except for LH, compared to PT (p < 0.05). GnRH and gonadotropin protein was also dynamically expressed across the estrous cycle and photoperiod exposure. The presence of cycling intraovarian GnRH-1 and gonadotropin mRNA suggests that these hormones may be locally involved in ovarian maintenance during SD regression and/or could potentially serve to prime ovaries for rapid recrudescence.General and Comparative Endocrinology 10/2010; 170(2):356-64. DOI:10.1016/j.ygcen.2010.10.008 · 2.47 Impact Factor