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PubMedDate not supplied

Endometrial biopsies during treatment with subcutaneous pulsatile gonadotropin-releasing hormone and luteal-phase human chorionic gonadotropin.

A high incidence of luteal phase defect (LPD) has been reported using subcutaneous pulsatile gonadotropin-releasing hormone for induction of ovulation. We reviewed all patients treated with the combination of subcutaneous pulsatile gonadotropin-releasing hormone during the follicular phase and human chorionic gonadotropin during the luteal phase (GnRH-hCG) who underwent endometrial biopsy during a treatment cycle. All of these patients had biopsy-proven LPD which persisted despite traditional therapy with progesterone vaginal suppositories and/or clomiphene citrate. The mean number of biopsies out of phase per patient prior to GnRH-hCG treatment was 2.8 +/- 0.2 (+/- SEM). When treated with GnRH-hCG, 15/16 patients (94%) showed a normal endometrial biopsy. The probability of this result occurring by chance alone allowing for a 50% treatment independent correction rate is less than .001. These results show that the combination of subcutaneous pulsatile gonadotropin-releasing hormone and luteal-phase human chorionic gonadotropin can result in normal endometrial maturation in a high percentage of cycles when administered as described. It appears to be an effective alternative to traditional treatment modalities for luteal phase defect should one be needed.

Biopsy, Needle↗

PubMed1984

Effect of tyrosine modification on the biological and immunological properties of equine chorionic gonadotropin.

The tyrosine residues of equine chorionic gonadotropin have been nitrated with tetranitromethane and the resulting effects on the biological and immunological activities of the hormone studied. All of the tyrosine residues in equine chorionic gonadotropin were found to react with tetranitromethane when a 100-fold molar excess of reagent was used or with an 8.6 molar excess in the presence of 5 M guanidine hydrochloride. Complete nitration abolished the biological activities and decreased the immunological activity of the hormone. The nitration of one tyrosine residue resulted in the loss of 70% of the LH activity of equine chorionic gonadotropin; the FSH activity declined in a similar fashion. Maximal nitration resulted in the loss of about 50% of the immunological activity of the native hormone. Nitrated derivatives of equine chorionic gonadotropin were unable to compete with the native hormone in the rat Leydig cell assay for LH. The results indicate that the tyrosine residues of equine chorionic gonadotropin play an important role in the manifestation of both the FSH and LH activity of the hormone.

Animals↗

PubMed1991

The luteal phase during gonadotropin therapy: effects of two human chorionic gonadotropin regimens.

OBJECTIVE: Luteal phase abnormalities are known to complicate ovulation induction with gonadotropins. This study was performed to test the effect of a modified human chorionic gonadotropin (hCG) regimen on the luteal phase during gonadotropin treatment. DESIGN: Fifteen women from a private practice setting volunteered to be studied during each of two nonconception, gonadotropin-stimulated cycles. After ovarian stimulation with human menopausal gonadotropins (hMG), hCG was administered either as a single dose of 10,000 IU (single dose) or in two divided doses of 5,000 IU given 1 week apart (split dose). MAIN OUTCOME MEASURES: Early, midluteal, and late luteal estradiol (E2) and progesterone (P) levels and luteal phase lengths were measured, and their median values and intraquartile ranges (IQR) compared using nonparametric analysis. RESULTS: Early and midluteal E2 and P levels were similar regardless of which hCG regimen was administered. The median late luteal E2 level was 1,146.0 pg/mL (the IQR ranged from 633 to 1,650, IQR = 1,017) with the split-dose regimen and 240.0 pg/mL (the IQR ranged from 150 to 460, IQR = 310) with the single-dose regimen. The median late luteal P level was 108.0 ng/mL (the IQR ranged from 58.5 to 129, IQR = 70.5) with the split-dose regimen and 4.2 ng/mL (the IQR ranged from 1.9 to 11.7, IQR = 9.8) with the single-dose regimen. Median luteal phase lengths were 16 days (the IQR ranged from 15 to 17, IQR = 2) for the split-dose regimen and 11 days (the IQR ranged from 10 to 12, IQR = 2) for the single-dose regimen. CONCLUSION: In hMG-stimulated cycles, a second dose of hCG given during the midluteal phase significantly increases late luteal E2 and P levels and consistently lengthens the luteal phase.

Adult↗

PubMed1995

Signaling and transacting factors in the transcriptional inhibition of gonadotropin releasing hormone gene by human chorionic gonadotropin in immortalized hypothalamic GT1-7 neurons.

We recently demonstrated that immortalized GT1-7 neurons co-express luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptor and gonadotropin releasing hormone (GnRH) genes. Treatment of GT1-7 neurons with LH/hCG resulted in a transcriptional inhibition of GnRH gene. In the present study, we investigated the signaling and transacting factors involved in the action of hCG. Eight-bromo-cyclic AMP can mimic the down-regulating action of hCG on GnRH mRNA levels. H-89, a protein kinase (PK) A inhibitor, but not bisindolylmaleimide, a PKC inhibitor, blocked the down- regulating actions of hCG as well as of 8-bromocyclic AMP. Treatment with the PKA inhibitor alone modestly decreased GnRH mRNA levels suggesting that PKA signaling also controls the basal expression of the GnRH gene. The direct measurement of PK activities revealed that hCG treatment of GT1-7 neurons increased the PKA but not the PKC activity. New protein synthesis is required for the down-regulating action of hCG on GnRH mRNA levels. Since some of the new proteins could be nuclear transcription or transacting factors, we investigated the effects of hCG on cyclic AMP response element binding protein (CREB), c-Fos and c-Jun protein levels. Treatment of GT1-7 neurons with hCG resulted in an increase of 43 kDa phosphorylated CREB, 50 kDa c-Fos and 40 kDa c-Jun proteins compared to the corresponding controls. The kinetics of increases were different and in all cases the increases of the proteins preceded the decrease of GnRH mRNA levels. In summary, PKA signaling and transacting factors such as CREB, Fos and Jun are probably involved in transcriptional inhibition of GnRH gene by hCG in GT1-7 neurons.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1993

Spontaneous and gonadotropin-releasing hormone induced human chorionic gonadotropin release from superfused JAR choriocarcinoma cells.

JAR choriocarcinoma cells have retained several characteristics of normal trophoblasts and have been used as an in vitro trophoblast model. The superfusion system is suitable for the study of hormone synthesis and/or secretion. JAR cells were cultured and transferred to the superfusion system in order to evaluate the spontaneous hCG secretion and the effect of GnRH. The spontaneous hCG release showed a periodic pattern with a 48 min phase interval. In our system single cells and cell-clusters were superfused and there is a possibility that cell to cell connections might have an influence on the regulation of hormone synthesis and/or secretion. GnRH in 4 x 10(-7) M and 4 x 10(-6) M concentrations or 100 mM KCl caused an immediate hCG release from the JAR cells Repeated administration of GnRH resulted in a delayed hCG release which is probably related to the relatively small amount of hCG available from the storage granules or to the phase of spontaneous secretion.

Cell Line↗

PubMed1988

Double immunoelectron microscopic labelings of human chorionic gonadotropin and human placental lactogen in human chorionic villi.

Simultaneous immunoelectron microscopic localization of human chorionic gonadotropin (HCG) and human placental lactogen (HPL) was examined on the same ultrathin section of human chorionic villi by means of the double labeling technique. Using specific rabbit antisera against HCG and HPL followed by goat anti-rabbit IgG-coated colloidal gold of different sizes (15 nm and 5 nm), immunoreactions of HCG were concentrated on middle-sized secretory granules of 200-300 nm and large dense bodies of 500-1000 nm, while those of HPL were exclusively located on small secretory granules of 80-180 nm. The present experiment provides direct evidence for our previous data that HCG and HPL seem to be stored in different granular components in the syncytiotrophoblast.

Chorionic Gonadotropin↗

PubMedDate not supplied

Uterine response to estradiol under action of chorionic gonadotropin in mice.

This work examined the effect of chorionic gonadotropin on proliferative and morphogenetic reactions in the uterus under short- and long-term estrogen treatments. Ovariectomized mice received a single injection with estradiol dipropionate (2 micro g per 100 g; subcutaneously, sc) or vehicle and injections with human chorionic gonadotropin (10 IU per 100 g; sc) or vehicle twice a day for 2 days. Other groups of animals received injections with estradiol once a week or vehicle and injections with chorionic gonadotropin or vehicle once a day for 30 days. The uteri were removed 48 h after the last estradiol or vehicle injection. In animals treated with estradiol and chorionic gonadotropin for a month, the incidence of atypical endometrial hyperplasia was significantly higher. In animals treated with estradiol and chorionic gonadotropin for 2 days or for a month, uterine mass was slightly increased, the number of mitotic cells and BrdU-labeled cells was greater in luminal epithelium, glandular epithelium, stromal and myometrial cells, whereas the expression of estrogen receptors-alpha was lower in all uterine compartments, than in control. In mice who received estradiol and chorionic gonadotropin for 2 days, levels of beta-catenin and glycogen synthase kinase-3beta in luminal and glandular epithelia were lower. In animals treated with estradiol and chorionic gonadotropin for a month, the level of beta-catenin was slightly higher, and the expression of glycogen synthase kinase-3beta was lower in luminal and glandular epithelia. Thus, chorionic gonadotropin exerts estradiol-induced proliferative and morphogenetic changes in the uterus. This action of chorionic gonadotropin is associated with decreased expression of estrogen receptors-alpha and with changes in expression of beta-catenin and glycogen synthase kinase-3beta in the uterus.

Animals↗

PubMed1994

Human chorionic gonadotropin secretion and protein phosphorylation in chorionic tissue.

The signal transduction system acts either monodirectionally (synergistically) or bidirectionally (antagonistically) in different tissues. We activated the signal transduction system in BeWo human choriocarcinoma cells and studied the effects on human chorionic gonadotropin (hCG) secretion, cell proliferation, and DNA synthesis. Protein phosphorylation in the cytosolic fraction was also studied by two-dimensional polyacrylamide gel electrophoresis. When phorbol 12-myristate 13-acetate (PMA) was added to cultures, hCG secretion was increased dose-dependently, but cell proliferation and 3H-thymidine uptake were not affected. When only cholera toxin was added, hCG secretion was also stimulated dose-dependently, but when both PMA and cholera toxin were added there was a synergistic potentiation of hCG production. In contrast, Ca ionophore A23187 had almost no effect on hCG secretion. Two-dimensional gel electrophoresis and autoradiography showed that phosphorylation of a 33 kd acidic protein was produced by cholera toxin, while phosphorylation of a 45 kd acidic protein and dephosphorylation of a 14 kd acidic protein were caused by the phorbol ester. These proteins may be specific substrates of protein kinase A and protein kinase C, respectively, in BeWo cells.

Cell Division↗

PubMed2002

False-positive serum human chorionic gonadotropin results: causes, characteristics, and recognition.

False-positive serum human chorionic gonadotropin results are estimated to occur in 1 in 10(3) to 1 in 10(4) tests. Most of these false-positive results are due to interference by non-human chorionic gonadotropin substances (especially human luteinizing hormone and anti-animal immunoglobulin antibodies) and the detection of pituitary human chorionic gonadotropin. The false-positive human chorionic gonadotropin measurements are characterized by serum levels that are generally <1000 mIU/mL, the absence of human chorionic gonadotropin in the urine, nonparallelism of the human chorionic gonadotropin levels in serial dilutions of the serum with the human chorionic gonadotropin standard, results that are not consistent with the clinical or operative findings, the absence of a substantial change in the serum levels over time or after therapy, and the finding of a negative result when an alternative type of human chorionic gonadotropin assay is used. An algorithm is presented to aid in the recognition of false-positive human chorionic gonadotropin results in patients.

Algorithms↗

PubMed1984

Ovulation induction with subcutaneous pulsatile gonadotropin-releasing hormone: the role of supplemental human chorionic gonadotropin in the luteal phase.

Four subjects with hypothalamic amenorrhea were administered subcutaneous pulsatile gonadotropin-releasing hormone (GnRH) for ovulation induction. GnRH was discontinued at the time of presumed ovulation in all cases. In the first two patients the luteal phase was supported with human chorionic gonadotropin in the initial cycle but not in the second cycle. In patient 3, the reverse was true. Patient 4 had only one cycle on GnRH, and it was unsupported. Daily blood samples were obtained for luteinizing hormone, follicle-stimulating hormone, estradiol, and progesterone (P); and frequent pelvic ultrasound examinations were performed. Presumed ovulation as determined by ultrasound occurred in all seven cycles. The first three patients had short luteal phases with poor P production in the unsupported cycles. However, the fourth patient, who had shown pituitary response in GnRH testing, had a normal luteal phase with good P production without human chorionic gonadotropin support. These data support the notion that subcutaneous pulsatile GnRH can be used for the induction of ovulation. However, if the luteal phase is not supported, an inadequate corpus luteum may result.

Amenorrhea↗

PubMed1975

Human chorionic gonadotropin. V. Tissue specificity of binding and partial characterization of soluble human chorionic gonadotropin-receptor complexes.

An in vivo human chorionic gonadotropin (hCG)-receptor complex was solubilized from the subcellular fraction of ovarian and testicular tissues of rats that had been injected with 125-I-labeled hCG. The soluble hCG-receptor complex was partially characterized by Sepharose 6B chromatography in the presence of the nonionic detergent, Emulphogene, and was shown to have a molecular size of about 65 A. By this method it was also shown that the in vivo uptake of radioactivity by rat gonadal tissues represents 125-I-hCG and not the dissociated subunits or degradation products of the hormone. A soluble hCG-receptor complex isolated in vitro in approximately the same yield from both rat testicular and ovarian homogenates was shown to be the same size. The hCG-receptor appears to be specifically located in gonadal tissue; a corresponding hCG-receptor complex was not obtained from liver or kidney that incorporated significant levels of 125-I-hCG administered in vivo. Furthermore, a desialyzed hCG-receptor complex was obtained from rat testis but not liver; desialyzed hCG, like other desialyzed glycoproteins, is nonspecifically bound by rat liver homogenates. The binding of hCG and luteinizing hormone (LH) by rat testis receptor exhibits a high degree of specificity. Other glycoprotein hormones without LH activity, such as follicle-stimulating hormone and thyroid-stimulating hormone, and glycoproteins such as fetuin or alpha1-acid glycoprotein do not bind to the hCG/LH receptors. Desialyzed hCG was 2 times more effective in competing for binding to rat testis receptors than "native" hCG, indicating that caution must be exercised when the radioligand receptor assay is utilized to assay hCG preparations varying in sialic acid content.

Animals↗

PubMed1988

High frequency of incomplete human chorionic gonadotropin in patients with testicular seminoma.

We measured human chorionic gonadotropin by 2 immunometric assays that require that the entire human chorionic gonadotropin molecule is intact, and by a competitive radioimmunoassay that measures intact human chorionic gonadotropin and its free beta-chain. The sera tested were samples from male cancer patients with elevated human chorionic gonadotropin levels obtained by the radioimmunoassay method. Elevated levels were confirmed in 67 of 92 samples (72 per cent) with the immunometric methods. However, in 25 of 97 patients (28 per cent) elevated human chorionic gonadotropin was found with the radioimmunoassay, whereas the values were in the normal range when measured with the immunometric assays. These discrepancies were found in 22 patients with seminomatous tumors, including 2 extragonadal germ cell tumors, which constitutes 42 per cent of all seminoma patients tested. Of the remaining 3 discrepant patients 2 had lung cancer and 1 had metastases from an unknown primary cancer.

Biomarkers, Tumor↗

PubMed1986

Increased rat testicular heme oxygenase activity associated with depressed microsomal heme and cytochrome P-450 levels after repeated administration of human chorionic gonadotropin.

Repeated administration of human chorionic gonadotropin to rats results in a maximal depression of testicular microsomal heme and cytochrome P-450 levels at 24 h, followed by increases that plateau at pretreatment levels by day six. Associated with the depressed levels of microsomal heme and cytochrome P-450 is an increase of testicular microsomal heme oxygenase activity at 12-24 h. Testicular mitochondrial delta-aminolevulinic acid synthase activity was increased at 24 h, and remained elevated throughout the 9-day treatment period. Pretreatment with 1,4,6-androstatrien-3,17-dione, an aromatase inhibitor, failed to prevent the depression of testicular microsomal heme or cytochrome P-450 or increased heme oxygenase activity caused by repeated administration of human chorionic gonadotropin, and administration of estradiol benzoate failed to alter testicular microsomal heme oxygenase activity suggesting that these parameters were not related to altered testicular estrogen content caused by increased aromatase activity. These results suggest that increased testicular heme oxygenase activity is associated with decreased microsomal heme and cytochrome P-450 content during human chorionic gonadotropin-induced desensitization.

5-Aminolevulinate Synthetase↗

PubMed1983

Effects of hyper- and hypoprolactinemia on gonadotropin secretion, rat testicular luteinizing hormone/human chorionic gonadotropin receptors and testosterone production by isolated Leydig cells.

The effect of prolactin (Prl) on gonadotropin secretion, testicular luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptors, and testosterone (T) production by isolated Leydig cells has been studied in 60-day-old rats treated for 4 days, 4 and 8 weeks with sulpiride (SLP), a dopaminergic antagonist, or for 4 days and 4 weeks with bromocriptine (CB), a dopaminergic agonist. Plasma Prl concentrations were significantly greater in the SLP groups (204 +/- 6 ng/ml) and lower in the CB groups (3.0 +/- 0.2 ng/ml) than those measured in the control groups (54 +/- 6 ng/ml). The plasma concentrations of gonadotropin were not affected by a 4-day treatment with SLP or CB, nor were they after a 4-week treatment with CB. However, the hyperprolactinemia induced by an 8-week treatment with SLP was associated with a reduced secretion of gonadotropin (LH, 16 +/- 4 vs. 35 +/- 6 ng/ml; FSH, 166 +/- 12 vs. 307 +/- 14 ng/ml). In SLP-induced hyperprolactinemia, a 30% increase in the density of the LH/hCG testicular binding sites was observed (178 +/- 12 fmol/mg protein), whereas a 60% decrease was measured in hypoprolactinemia (55 +/- 5 vs. control 133 +/- 5 fmol/mg protein). Plasma T levels were increased in 4-day and 4-week hyperprolactinemic animals (4.3 +/- 0.4 and 3.9 +/- 0.4 ng/ml, respectively), but returned to normal levels in the 8-week group (3.0 +/- 0.5 vs. C: 2.3 +/- 0.2 ng/ml). No T modifications were observed in hypoprolactinemic animals. Two distinct populations of Leydig cells (I and II) were obtained by centrifugation of dispersed testicular cells on a 0-45% continuous Metrizamide gradient. Both possess LH/hCG binding sites. However, the T production from Leydig cells of population II increased in the presence of hCG, whereas that of cell population I which also contain immature germinal cells did not respond. The basal and stimulated T secretions from cell populations I and II obtained from CB-treated animals were similar to controls, whereas from 4 days to 8 weeks of hyperprolactinemia, basal and hCG induced T productions from cell population II decreased progressively. These data show that hyperprolactinemia causes, in a time-dependent manner, a trophic effect on the density of LH/hCG testicular receptors; reduces basal and hCG-stimulated T production from isolated Leydig cells type II; and results in an elevated plasma T concentration which decreases with time. The latter suggests a slower T catabolism and/or an impaired peripheral conversion of T into 5 alpha-dihydrotestosterone (DHT). Although hypoprolactinemia is associated with a marked reduction in testicular LH receptors, it does not affect T production.

Animals↗

PubMed2000

Role of potassium ions in monocyte-regulating effects of chorionic gonadotropin.

We studied the effects of chorionic gonadotropin on intracellular K(+)content and phagocytic activity of human peripheral blood monocytes. Since the immunomodulating properties of chorionic gonadotropin are known to depend on female sex steroids, the phase of the menstrual cycle was taken into account. Chorionic gonadotropic modulated the content of intracellular K(+)and phagocytic activity of monocytes. These changes were most pronounced under the effect of chorionic gonadotropin in high physiological doses (100 U/ml) and depended on the phase of the menstrual cycle. A direct correlation was found between elevation of K(+)content in monocytes and activation of phagocytosis during the luteal phase.

Cations, Monovalent↗

PubMed2000

Hormone interactions to Leu-rich repeats in the gonadotropin receptors. III. Photoaffinity labeling of human chorionic gonadotropin with receptor Leu-rich repeat 4 peptide.

Human chorionic gonadotropin (hCG) binds to the extracellular N-terminal domain, exodomain, of its receptor, and the resulting hCG-exodomain complex is thought to modulate the membrane associated domain, endodomain, of the receptor to generate hormone signal. The bulk of the exodomain is speculated to assume a crescent structure consisting of eight to nine Leu-rich repeats (LRRs), which may provide the hormone contact sites. Unfortunately, little experimental evidence is available for the precise hormone contact points in the exodomain and the endodomain. The two preceding articles (Song, Y., Ji, I., Beauchamp, J., Isaacs, N., and Ji, T. (2001) J. Biol. Chem. 276, 3426-3435; Song, Y., Ji, I., Beauchamp, J., Isaacs, N., and Ji, T. (2001) J. Biol. Chem. 276, 3436-3442) show that putative LRR2 and LRR4 are crucial for hormone binding. In particular, the N-terminal region of LRR4 assumes the hydrophobic core of the LRR4 loop, whereas the C-terminal region is crucial for signal generation. However, it is unclear whether LRR4 interacts hCG and the endodomain and how it might be involved in signal generation. In this article, our affinity labeling results present the first evidence that the N-terminal region of LRR4 interacts with hCG, preferentially the hCGalpha subunit and that the hCG/LRR4 complex interacts with exoloop 2 of the endodomain. This interaction offers a mechanism to generate hormone signal.

Amino Acid Motifs↗

PubMed1977

Gonadotropin-inhibitory contaminants in partially purified pharmaceutical preparations of human chorionic gonadotropin.

Various commercial preparations of partially purified human chorionic gonadotropin, inactivated by heating, inhibited the uterine growth induced in immature mice with the same active gonadotropins as well as spontaneous uterine growth. The more purified preparations of chorionic gonadotropin failed to produce these effects after inactivation by boiling, suggesting that the inhibitory activity is not generated from gonadotropin by the procedure but may be related to some contaminant similar to the gonadotropin-inhibitory substance previously found in human urine.

Animals↗

PubMed1984

Human chorionic gonadotropin testing. Changing testicular response in infants with microphallus and gonadotropin deficiency.

The evaluation of microphallus often includes human chorionic gonadotropin (HCG) stimulation to evaluate testicular androgen production. The response in testosterone secretion after five days of stimulation with chorionic gonadotropin is abnormal in patients with either primary testicular defects or gonadotropin deficiency. The testes of gonadotropin-deficient children do respond if the chorionic gonadotropin therapy is continued for six weeks. The current study reports a normal response to the short course (five days) of chorionic gonadotropin therapy in two 2-month-old patients with XY chromosomes with microphallus whose clinical course and repeated testing at age 3 or 4 years indicated gonadotropin deficiency. The normal response in the neonatal period is probably the result of maternal chorionic gonadotropin priming of the fetal testes in utero. These results indicate that HCG testing is an unreliable method for identifying gonadotropin deficiency in the neonatal period.

Abnormalities, Multiple↗