No Abstract Available.
Gonadotropin-Releasing Hormone* ; Receptors, LHRH*

OBJECTIVESTo study the coexistence of androgen receptor(AR) and GnRH receptor(GnRHR), and further identify that submaxillary is a target organ of androgen and GnRH in SD Rat.

METHODSSequential deparaffinized sections of SD rat submaxillary were immunostained with SABC method. The first antibodies were rabbit anti-rat GnRH idiotypic antibodies and mouse anti-rat androgen receptor antibodies.

RESULTSAR immunoreactive cells were found in glandular epithelial cells of serous acinus and epithelial cells in all gland ducts. While the distribution of GnRHR coincides with that of AR. The immunoreactive substances were distributed in cytoplasm of all positive cells with negative nuclei.

CONCLUSIONSThe results showed that AR existed in submaxillary and was widely distributed in glandular epithelial cells with distributive pattern similar to those of GnRHR. It suggests that submaxillary is a target organ of androgen, responsible for modulating biological function of submaxillary.

Animals ; Immunohistochemistry ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, Androgen ; metabolism ; Receptors, LHRH ; metabolism ; Submandibular Gland ; metabolism

Isolated gonadotropin deficiency can be idiopathic or a part of X-linked Kallmann syndrome associated with anosmia. There have been several trials to reveal the genetic mutations that affect gonadotropin secretion, and approximately 10% of sporadic patients have mutations in either gonadotropin releasing hormone receptor (GnRHR) or KAL1 gene. Here we report one familial cases of idiopathic hypogonadotropic hypogonadism occurred in a boy and his elder sister. They presented with delayed puberty and hypoplastic gonads, but normal sense of smell. We performed GnRHR and KAL1 mutation analysis, but could not find any mutation.
Gonadotropins ; Gonads ; Humans ; Hypogonadism* ; Kallmann Syndrome ; Male* ; Olfaction Disorders ; Puberty, Delayed ; Receptors, LHRH ; Siblings* ; Smell

OBJECTIVETo investigate ovarian follicular damage induced by chemotherapeutic agents and gonadotropin- releasing hormone receptor (GnRHR) expression in the damaged ovaries in rats.

METHODSTwo groups of adult SD rats were subjected to intraperitoneal injection of a single-dose cyclophosphamide and saline, respectively, and 8 weeks later, the ovaries were taken for observing the ovarian damages. The distribution of GnRHR was detected with immunohistochemistry, and RT-PCR was used to determine the expression of GnRHR mRNA in the rat ovaries.

RESULTSMassive primordial follicular loss occurred in the ovaries of rats exposed to cyclophosphamide with also evident stromal ovarian blood vessel damages and focal fibrosis. Both the protein and mRNA expressions of GnRHR were detected in normal rat ovaries, but in rats exposed to cyclophosphamide, the expressions were significantly lowered in the ovaries (P<0.05).

CONCLUSIONLow-level GnRHR expressions in the ovaries of rats with cyclophosphamide exposure suggest microenvironment disturbances in the damaged rat ovaries in advanced stage of chemotherapy.

Animals ; Cyclophosphamide ; adverse effects ; Female ; Humans ; Ovary ; drug effects ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Receptors, LHRH ; metabolism

Uterine fibroids (leiomyomas or myomas), benign monoclonal tumors, are the most common benign tumors in women. Heavy or prolonged menstrual bleeding, abnormal uterine bleeding, resultant anemia, pelvic pain, infertility, and/or recurrent pregnancy loss are generally associated with uterine fibroids. Although curative treatment of this tumor relies on surgical therapies, medical treatments are considered the first-line treatment to preserve fertility and avoid or delay surgery. The aim of this review is to provide available and emerging medical treatment options for symptomatic uterine fibroids. Literature review and consensus of expert opinion. Many uterine fibroids are asymptomatic and require no intervention, although it is advisable to follow-up patients to document stability in size and growth. Fibroid-associated symptoms include heavy menstrual bleeding and pain or pelvic discomfort. The association between infertility and fibroids increases with age. Treatment options for symptomatic uterine fibroids — include medical, surgical, and radiologically guided interventions. Various medical therapies are now available for women with uterine fibroids, although each therapy has its own advantages and disadvantages. Currently, gonadotrophin-releasing hormone (GnRH) agonists and selective progesterone receptor modulators (SPRMs) are the most effective medical therapies, with the most evidence to support their reduction of fibroid volume and symptomatic improvement in menstrual bleeding. The choice of treatment depends on the patient's personal treatment goals, as well as efficacy and need for repeated interventions.
Anemia ; Consensus ; Expert Testimony ; Female ; Fertility ; Follow-Up Studies ; Hemorrhage ; Humans ; Infertility ; Leiomyoma* ; Pelvic Pain ; Pregnancy ; Receptors, LHRH ; Receptors, Progesterone ; Uterine Hemorrhage

Animals ; Diethylhexyl Phthalate ; toxicity ; Female ; Ovary ; drug effects ; metabolism ; ultrastructure ; Rats, Sprague-Dawley ; Receptors, LH ; metabolism ; Receptors, LHRH ; metabolism ; Toxicity Tests

PURPOSE: Gonadotropin-releasing hormone (Gn-RH) can cause regression of hormonedependent human tumors, including uterine endometrial and ovarian carcinomas. These effects were thought to be mediated through the inhibition of gonadotropic and steroid hormone from the hypothalamus. But, in addition to its classic hypophysiotropic action, Gn-RH might play a role as a modulator of activity in the brain and many peripheral organs. It has been reported that this analog has a direct inhibitory effect on the tumor and that the specific binding sites for Gn-RH were demonstrated in certain tumors responsive to Gn-RH. In support of a possible clinical use of Gn-RH analogs in the treatment of the endometrial and ovarian carcinomas, we tried to find out whether Gn-RH receptors are present on hormone dependent tumors. MATERIALS AND METHODS: We have studied endometrial and ovarian tumor specimens and established uterine endometrial and ovarian carcinoma cell lines for the presence of Gn-RH receptor by the detection of its messenger ribonucleic acid (mRNA). We also compared the results obtained from tumor tissue specimens with the results from their corresponding normal tissues. Gn-RH receptor mRNA was determined by reverse transcription-polymerase chain reaction using oligonucleotide primers synthesized according to the published human Gn-RH receptor sequence. RESULTS: Gn-RH receptor mRNA was detected in all normal endometrium and abnormally proliferative endometrium presenting dysfunctional bleeding, but not all in endometrial carcinomas (83%). Tumor stage and histologic grading had no relationship with receptor positivity. And, Gn-RH receptor mRNA was detected in less than 40% in normal myometrium and myomas. Gn-RH receptor expression was detected in same frequencies (86%) in normal ovarian tissues and ovarian carcinomas. Receptors were detected in a high proportion of the specimens from epithelial carcinomas (92%) and stromal tumors (100%) of the ovary. But, Gn-RH receptor was not detected in germ-cell derived tumors of the ovary. Established endometrial carcinoma (CUME-1) and epithelial ovarian carcinoma (CUMO-2) cell lines also demonstrated Gn-RH receptor mRNA, respectively. CONCLUSIONS: The expression of Gn-RH receptor raises the possibility that Gn-RH may play a direct regulatory role in the growth of hormone-dependent normal tissues and their respective tumors, and provides a possible point of attack for therapeutic approaches using Gn-RH analogs in endometrial and ovarian malignancies.
Animals ; Binding Sites ; Brain ; Cell Line ; DNA Primers ; Endometrial Neoplasms ; Endometrium ; Female ; Gonadotropin-Releasing Hormone* ; Hemorrhage ; Humans* ; Hypothalamus ; Mice ; Myoma ; Myometrium ; Ovary ; Receptors, LHRH* ; RNA ; RNA, Messenger

Gonadotropin releasing hormone (GnRH) is believed to be pivotal hormone in hypothalamo-pituitary gonadal axis and the hypothalamus is believed as the exclusive organ producing GnRH and pituitary is for GnRH re ceptor until recently. Some reported the exptra-hypothalamic GnRH or extra-pituitary GnRH receptors from decades ago. The aims of this study are to confirm the existence of the GnRH receptor in bladder epithelial cancer cell, HT-1197 and HT-1376, and evaluated the possible role of the GnRH on cell cycle. The GnRH and GnRH receptor were detected by immunohistochemical staining and the effect of GnRH on cell cycle change in both cell line were studied by fluorescence activated cell sorter (FACS). The control cells were cultured at media supplemented with normal serum, and experimental group were cultured at media supplemented with charcoal stripped serum (CSS) which excluding peptide hormones except exogenous GnRH with different concentration. The GnRHs and GnRH receptors were detected at both cell lines and the cell cycle analysis showed that there were little difference in proportion of cell cycle among examined 10,000 cells in both cell lines, neither control nor experimental groups. This study shows that the GnRHs and GnRH receptors exist in bladder cancer cells and GnRH did not influence on the cell cycle progression. With this study, we suppose that the bladder cancer cells produce the GnRH and GnRH receptors and the role of the GnRF produced from the bladder cancer cells might be the autocrine rather than endo-or paracrine factor.
Axis, Cervical Vertebra ; Cell Cycle* ; Cell Line ; Charcoal ; Fluorescence ; Gonadotropin-Releasing Hormone* ; Gonadotropins* ; Gonads ; Hypothalamus ; Peptide Hormones ; Receptors, LHRH ; Urinary Bladder ; Urinary Bladder Neoplasms

BACKGROUND: Kallmann's syndrome is related to the defect in migration of olfactory neuron and GnRH neuron from the olfactory placode to the brain and it represents hypogonadism with anosmia or hyposmia. There are 3 modes of transmission in Kallmann's syndrome: X-linked, autosomal recessive and autosomal dominant. X-linked form is the most common. KAL gene is responsible for the X-linked form of Kallmann's syndrome and it had been localized to Xp22.3. The intron-exon organization had been determined and KAL gene mutation had also been identified in familial Kallmann's syndrome and it is very rare and shows heterogeneity. Furthermore, in the sporadic cases, KAL gene mutation is more rare. METHODS: In order to investigate the KAL gene mutation and the regulation of the gene expression in Kallmann's syndrome, we examined genomic DNA of 35 patients with sporadic Kallmann's syndrome. In the exon 3, 4, 5, 6, 7, 8, 9, 10, 11, 12 of KAL gene and 1, 2, 3 of GnRH receptor gene, the mutations were analyzed by PCR-based DNA sequencing. RESULTS: In our study, the mutation of KAL gene and GnRH receptor gene was not identified in the studied exons that were known as preferable sites of the mutation. CONCLUSION: The mutation of KAL gene and GnRH receptor gene is rare, and it might be needed to investigate mutations in other genes or in other part of the KAL gene such as intron or promoter region.
Brain ; DNA ; Emigration and Immigration ; Exons ; Gene Expression ; Gonadotropin-Releasing Hormone* ; Humans ; Hypogonadism ; Introns ; Kallmann Syndrome* ; Neurons ; Olfaction Disorders ; Population Characteristics ; Promoter Regions, Genetic ; Receptors, LHRH* ; Sequence Analysis, DNA

PURPOSE: To confirm the production of extra-hypothalamic gonadotropin releasing hormone (GnRH) and GnRH receptor in bladder mucosal epithelia, and a potential role of GnRH on the bladder, normal human bladder tissues, and primary cultured dog bladder mucosal epithelia were studied. MATERIALS AND METHODS: For this study, normal human bladder tissue from 4 patients and primary cultured normal bladder mucosal epithelial cells from 2 dogs were used. For localization of extra-hypothalamic GnRH and the extra-pituitary GnRH receptor, in situ hybridization and immunohistochemical staining were done. To evaluate the roles of exogenous GnRH in bladder mucosal cells, the culture media were supplemented with charcoal stripped serum and 4 different concentrations of GnRH (0, 10(-3), 10(-5) and 10(-7)M). The effect of exogenous GnRH was evaluated using a hemocytometer and fluorescence activated cell sorter (FACS). RESULTS: GnRH and GnRH receptors, and their mRNA signals were localized in most of the both human bladder mucosal epithelia and dog bladder mucosal epithelia, but not in a few cells. There were no significant GnRH effects on cellular proliferation and cell cycle changes (p<0.05). CONCLISIONS: Bladder mucosal epithelium produces GnRH and GnRH receptors, but they do not effect either the proliferation or cell cycle changes. Although the exact function of extra-hypothalamic bladder GnRH is unknown, GnRH and GnRH receptors would be assumed to have unknown autocrine or paracrine relationships with each other.
Animals ; Cell Cycle ; Cell Proliferation ; Charcoal ; Culture Media ; Dogs ; Epithelial Cells ; Epithelium ; Fluorescence ; Gonadotropin-Releasing Hormone* ; Gonadotropins* ; Humans ; In Situ Hybridization ; Mucous Membrane ; Receptors, LHRH* ; RNA, Messenger ; Urinary Bladder*