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At least 109 records · Page 6Linked to original sources
PubMed1984

Modulation of cyclic AMP formation and progesterone secretion by human chorionic gonadotropin, epinephrine, buserelin and prostaglandins in normal or human chorionic gonadotropin desensitized rat immature luteal cells in monolayer culture.

It is now well recognized that hCG-induced luteolysis is associated with hCG-induced desensitization, but the physiological significance of luteal cell GnRH, PGs and beta-receptors is still undefined. Therefore, we intend in this study to observe the effects of prostaglandin F2 alpha and prostaglandin E2 and the interactions between epinephrine, a potent LHRH agonist [(D-Ser-(TBu)6, des-Gly-NH10(2) LHRH ethylamide: Buserelin] and hCG in normal and in vitro hCG-desensitized rat immature luteal cells in monolayer culture, on basal, hCG or cholera toxin stimulated intracellular and extracellular cAMP and progesterone secretion. The present report shows that incubation of immature rat luteal cells in monolayer culture with Buserelin, led to 25-50% inhibition of the epinephrine-as well as PGE2-induced cAMP and progesterone responses. The LHRH agonist can also reverse the stimulatory effects of cholera toxin in the presence of hCG and led with PGF2 alpha, to additive inhibitory effects on extracellular cAMP accumulation induced by cholera toxin. Both Buserelin and PGF2 alpha can reverse the hCG-induced cAMP and progesterone release but no effect could be observed when the incubation was carried out with either substance in the absence of hCG. Prostaglandin E2, in acute conditions of incubation, seems to share agonist properties with hCG when both were incubated with luteal cells. Buserelin reversed the stimulatory effects of PGE2, hCG, epinephrine and cholera toxin on cAMP and progesterone responses to these substances. These results suggest that Buserelin and PGF2 alpha have luteolytic-like effects and that there may be a complementary action for the two substances. Preincubation of rat luteal cells in monolayer culture with 1 nM hCG for a 24 h period led to the inhibition of cAMP and progesterone responses after a subsequent exposure to hCG and epinephrine. Luteal cells were no longer responsive to hCG while the presence of epinephrine in hCG-desensitized cells led to a 40% stimulation of cAMP and progesterone production. These observations suggest that occurred a partial alteration of the N component activity of the adenylyl cyclase system.

Animals↗
PubMed1984

Modulation of cyclic AMP formation and progesterone secretion by human chorionic gonadotropin, epinephrine, buserelin and prostaglandins in normal or human chorionic gonadotropin desensitized rat immature luteal cells in monolayer culture.

It is now well recognized that hCG-induced luteolysis is associated with hCG-induced desensitization, but the physiological significance of luteal cell GnRH, PGS and beta-receptors is still undefined. Therefore, we intend in this study to observe the effects of prostaglandin F2 alpha and prostaglandin E2 and the interactions between epinephrine, a potent LHRH agonist [(D-Ser-(TBu)6, des-Gly-NH2(10)) LHRH ethylamide: Buserelin] and hCG in normal and in vitro hCG-desensitized rat immature luteal cells in monolayer culture, on basal, hCG or cholera toxin stimulated intracellular and extracellular cyclic AMP and progesterone secretion. The present report shows that incubation of immature rat luteal cells in monolayer culture with Buserelin, led to 25-50% inhibition of the epinephrine--as well as PGE2--induced cyclic AMP and progesterone responses. The LHRH agonist can also reverse the stimulatory effects of cholera toxin in the presence of hCG and led with PGF2 alpha, to additive inhibitory effects on extracellular cyclic AMP accumulation induced by cholera toxin. Both Buserelin and PGF2 alpha can reverse the hCG-induced cyclic AMP and progesterone release but no effect could be observed when the incubation was carried out with either substance in the absence of hCG. Prostaglandin E2, in acute conditions of incubation, seems to share agonist properties with hCG when both were incubated with luteal cells. Buserelin reversed the stimulatory effects of PGE2, hCG, epinephrine, and cholera toxin on cyclic AMP and progesterone responses to these substances. These results suggest that Buserelin and PGF2 alpha have luteolytic-like effects and that there may be a complementary action for the two substances. Preincubation of rat luteal cells in monolayer culture with 1 nM hCG for a 24 h period led to the inhibition of cyclic AMP and progesterone responses after a subsequent exposure to hCG and epinephrine. Luteal cells were no longer responsive to hCG while the presence of epinephrine in hCG-desensitized cells led to a 40% stimulation of cAMP and progesterone production. These observations suggest that there occurred a partial alteration of the N component activity of the adenylyl cyclase system.

Animals↗
PubMed1979

Ovarian responses of pregnant mare serum gonadotropin- and human chorionic gondotropin-primed rats: desensitizing, luteolytic, and ovulatory effects of a single dose of human chorionic gonadotropin.

We conducted a study to determine the morphological appearance and functional responsiveness of ovarian tissues after administration of hCG to 28-day-old rats primed 65 h earlier with PMS gonadotropin (PMSG) and after administration of a second dose of hCG 5 days later, i.e. to 33-day-old rats containing heavily luteinized ovaries. Sixty-five hours after the administration of 50 IU PMSG sc to 25-day-old rats, ovaries already contained an abundance of luteinized follicles and an adenylyl cyclase (AC) system that was responsive to LH, epinephrine, and NaF. The administration of 50 IU hCG sc at this time initially resulted in a loss of LH-responsive ovarian AC. Within 4 days of the hCG injection, the ovaries of the now 32-day-old rats were heavily luteinized, and ovarian AC was highly responsive to LH, epinephrine, and NaF. The administration of a single sc dose of 200 IU hCG to 33-day-old PMSC- and hCG-primed rats with luteinized ovaries resulted in a rapid desensitization of the ovarian AC to LH and a drop in serum progesterone levels, During the subsequent 7 days, serum progesterone levels continued to decline, while total ovarian AC reacquired responsiveness to LH by days 4--5 after the densensitizing dose of hCG. Dissection of ovarian components revealed, however, that the AC system of the corpora lutea originally present at the time of the second hCG injection remained permanently refractory to LH and that the AC in corpora lutea newly formed from freshly ovulated follicles exhibited a significant responsiveness to LH, epinephrine, and NaF. However, these new corpora lutea were not fully active, since serum progesterone never rose. Subcutaneous administration of 50 IU hCG to 33-day-old PMSG- and hCG-primed rats also promoted a rapid loss of AC responsiveness to LH. This lower concentration of hCG was not sufficient to promote follicular development or ovulation, and the ovarian AC remained refractory to LH for at least 7 days. Intravenous administration of 75 IU hCG to 33-day-old PMSG- and hCG-primed rats similarly promoted a rapid and permanent loss of luteal AC responsiveness to LH; again, follicles did not mature to a preovulatory state and, in fact, appeared to undergo atresia rather than ovulation. These results indicate that in heavily luteinized ovaries 1) hCG promotes desensitization of rat luteal AC to LH, 2) Desensitization of AC to LH stimulation in corpora lutea is permanent and irreversible, and 3) only under conditions where follicles mature and ovulate and new corpora lutea are formed does total ovarian AC reacqure responsiveness during the subsequent week.

Adenylyl Cyclases↗
PubMed1989

Inhibin and activin modulate the release of gonadotropin-releasing hormone, human chorionic gonadotropin, and progesterone from cultured human placental cells.

Although it is clear that human chorionic gonadotropin (hCG) and progesterone play fundamental roles in pregnancy, the regulation of placental production of these hormones remains to be defined. Recent evidence suggests that the human placenta expresses proteins related to inhibin (alpha beta subunits) or activin (beta beta subunits). Inhibin and activin (follicle-stimulating hormone-releasing protein) possess opposing activities in several biological systems including pituitary follicle-stimulating hormone (follitropin) secretion, erythroid differentiation, and gonadal sex-steroid production. The actions of purified inhibin and activin on hormonogenesis by primary cultures of human placental cells were studied. The addition of activin increased gonadotropin-releasing hormone (GnRH) and progesterone production and potentiated the GnRH-induced release of hCG. Inhibin by itself did not modify placental immunoreactive GnRH, hCG, and progesterone secretion but reversed the activin-induced changes. Neither inhibin nor activin influenced the release of human placental lactogen. Furthermore, transforming growth factor beta, structurally related to inhibin/activin, did not significantly influence hormone release from cultured placental cells. These results support the hypothesis that inhibin and activin may play a role in regulating the release of GnRH, hCG, and progesterone from placenta and implicate inhibin-related proteins in the endocrine physiology of human pregnancy.

Activins↗
PubMed1984

Preliminary report about a modified gonadotropin (human menopausal gonadotropin/human chorionic gonadotropin) treatment in infertile patients with premature luteinization.

Premature luteinization is a frequent phenomenon observed in infertile women undergoing human menopausal gonadotropin/human chorionic gonadotropin (hMG/hCG) therapy for corpus luteum insufficiency or anovulatory cycles. By inducing hyperprolactinemia in these women with sulpiride, we intended to create a dysfunctional state in these women, which supposedly induces a better reaction to hMG/hCG therapy. The rationale behind this combined treatment was the observation that hyperprolactinemic amenorrheic patients have a much higher pregnancy rate under hMG/hCG treatment than the above group. Three cases are reported in detail, illustrating the altered ovarian response to combined sulpiride-hMG/hCG treatment. Of 60 infertile women with repeated premature luteinization, 12 conceived after sulpiride-hMG/hCG therapy. Their expected pregnancy rate would have been very low (5% or less) if conventional hMG/hCG treatment had been continued.

Adult↗
PubMed1985

Plasma prorenin in first-trimester pregnancy: relationship to changes in human chorionic gonadotropin.

Prorenin and human chorionic gonadotropin are both synthesized in chorionic cells. The relationship of changes in maternal plasma prorenin to changes in human chorionic gonadotropin were therefore evaluated during the first trimester. In samples submitted to the routine chemistry laboratory for detection of pregnancy a positive relationship was observed between prorenin and beta human chorionic gonadotropin during the 5 weeks following conception. Subsequently human chorionic gonadotropin continued to rise but prorenin had reached a plateau. Serial studies in one subject demonstrated that prorenin had increased to 65% of maximum by the thirteenth day following conception whereas human chorionic gonadotropin had risen to only 0.2% of maximum. By 3 to 5 days post partum, beta human chorionic gonadotropin had fallen by 98% but prorenin had fallen by only 50%. The early rise in prorenin following conception and the relatively slow fall post partum suggest that pregnancy-related changes in maternal plasma prorenin are of maternal, not fetal, origin.

Chorionic Gonadotropin↗
PubMed2007

Interventions after artificial insemination: conception rates, pregnancy survival, and ovarian responses to gonadotropin-releasing hormone, human chorionic gonadotropin, and progesterone.

We hypothesized that increasing concentrations of progesterone (P4) after artificial insemination would increase fertility. Our objective was to assess changes in ovarian structures, incidence of ovulation, and change in serum P4 in response to GnRH, human chorionic gonadotropin (hCG), or exogenous P4 (controlled internal drug release; CIDR insert) treatment beginning 4 to 9 d after artificial insemination (d 0) and again 7 d later (experiment 1). Blood was collected from 753 cows in 3 herds on d 0 and 7. Ovaries of 162 cows were scanned and mapped to confirm the presence of a corpus luteum (CL), and cows were assigned randomly to serve as controls (n = 41) or to receive a CIDR insert for 7 d (n = 41), 100 microg of GnRH (n = 40), or 3,300 IU of hCG (n = 40). More cows were induced to ovulate in response to GnRH (60%) and hCG (78%) compared with controls (2.4%). Compared with controls, cows treated with GnRH or hCG had more induced CL (d 7) and more total CL (d 7), but serum P4 was increased only in response to hCG. Largest follicle diameters on d 7 were less after GnRH and hCG, but total follicular volume on d 7 was reduced by GnRH, hCG, and CIDR, compared with that of controls. Volume of the original luteal structures was increased by hCG but tended to be reduced by CIDR and GnRH compared with luteal volume in controls. Total CL volume was increased by hCG, but reduced by CIDR, compared with CL volume of controls. Conception rates and pregnancy survival were assessed in response to the same treatments described in experiment 1: controls (n = 708), CIDR (n = 711), GnRH (n = 719), and hCG (n = 714). Tendencies for interactions of treatment x herd and treatment x lactation group were detected, but no 3-way interactions were found. Treatment with hCG increased conception rates in second-lactation cows. The CIDR tended to increase, and hCG increased, conception rates in 2 herds, whereas the CIDR decreased conception rates in 1 herd. Pregnancy survival was reduced by GnRH compared with that in controls. We concluded that GnRH and hCG effectively induced ovulation, and increased number of CL, but only increased serum P4 in hCG-treated cows. Further, treatment with the CIDR or hCG increased conception rates but only in some herds.

Animals↗
PubMed1991

Goat antibodies to amino acid sequences of human chorionic gonadotropin (hCG)

Human chorionic gonadotropin, its two subunits and its conjugate with thyroglobulin were used for immunization. The strongest immunogens were demonstrated to be the intact hormone and beta subunit, the weakest was alpha subunit. Using three peptides corresponding to hormone subunits coupled to Sepharose 4B various antibodies were isolated from goat antiserum by immunoaffinity chromatography. Specificity of the purified antibody preparations was studied. It was demonstrated that enzyme linked immunosorbent assay with two goat antibodies--one for coating of microtiter plates and the other one conjugated with peroxidase--is suitable for sensitive assays of both human chorionic gonadotropin and luteinizing hormone. Specific and sensitive assays were performed using combination of goat antibody anti-122-145-beta hCG and monoclonal antibody anti-alpha hCG.

Amino Acid Sequence↗
PubMed1999

Autoradiographic analysis of follicle-stimulating hormone and human chorionic gonadotropin receptors in the ovary of immature rats treated with equine chorionic gonadotropin.

The gonadotropin-primed immature rat has become the most common model for the study of follicular development and ovulation. In this study, prepubertal female rats, 23 and 24 days old, were injected s. c. with 5 IU eCG, and ovaries were collected for topical autoradiography of FSH and hCG receptors at 48 or 24 h post-eCG, respectively (i.e., Day 25). In a baseline group, on Day 25 (before eCG), even the smallest preantral follicles with 1 layer of granulosa cells (GCs; primary follicles) possessed FSH receptors, but hCG receptors were found only on the theca of follicles with 2 or more layers of GCs. Human CG receptors were especially prominent in the interstitium that intimately surrounds preantral follicles without any distinction between theca and interstitial cells. There was a discrete theca surrounding antral follicles. Occasionally antral follicles had hCG receptors in the interstitium, but the adjacent theca was negative, suggesting that these follicles might be destined for atresia. By 24 h post-eCG, a now-discrete theca layer with hCG receptors surrounded all preantral follicles except for the primary follicles, which never responded to eCG. The interstitium was hypertrophied and epithelioid, as was the theca surrounding nonatretic preantral and antral follicles. Increased mitotic activity characterized the growing preantral follicle, and for the first time, FSH binding in GCs of antral follicles was greater than in the preantral population. By 48 h post-eCG, the primary follicles were still unresponsive to eCG. FSH receptors were even more pronounced in the GCs of large antral follicles, although hCG receptors were present in the GCs of only one third of the antral follicles, reflecting the small dose of eCG administered. By 48 h post-eCG, receptors in the interstitium were barely detectable. Using this model, the following study considers the functional in vitro changes in steroidogenesis in follicles from the smallest preantral follicles to the largest antral follicles.

Animals↗
PubMed1990

Detection of a small molecular species of human chorionic gonadotropin in the urine of patients with carcinoma of the cervix and cervical intraepithelial neoplasia: comparison with other assays for human chorionic gonadotropin and its fragments.

A low-molecular-weight glycoprotein containing sequences of the beta subunit of human chorionic gonadotropin (hCG) has been found in the urine of patients with carcinoma of the cervix using an immunoradiometric assay. This fragment has chromatographic and immunological identity with hCG beta core. This molecule was present in 52 to 77% of all patients with invasive disease, while between 11 and 27% of patients with cervical intraepithelial neoplasia (CIN) also exhibited significant hCG beta-core immunoactivity. Few patients had either a positive assay for intact hCG or a positive assay directed at an epitope on the beta subunit (beta-hCG radioimmunoassay) in serum. However, between 17 and 40% of patients with invasive disease were positive for free beta-subunit immunoactivity in the blood. The origin of the beta-core immunoactivity in the urine is uncertain; while tumor production cannot be excluded, it is possible that the molecule originates from renal metabolism of small quantities of the beta subunit of hCG. Regardless of the source of the molecule, hCG beta core is a far more sensitive marker of hCG production by tumors than is serum hCG.

Carcinoma↗
PubMed2004

Expression and regulation of luteinizing hormone/human chorionic gonadotropin receptors in ovarian cancer and its correlation to human chorionic gonadotropin-doxorubicin sensitivity.

OBJECTIVE: Ovarian cancer cell lines and tissues express gonadotropin receptors. Conjugation of cytostatics to ligands of these receptors may increase the specificity of cytotoxic drugs. STUDY DESIGN: Toxicity of doxorubicin-human chorionic gonadotropin conjugates was determined in 4 ovarian cancer cell lines. Expression and regulation of luteinizing hormone/human chorionic gonadotropin receptors were analyzed before and after treatment with human chorionic gonadotropin, epidermal growth factor, and 8-bromo-cyclic adenosine monophosphate with a nested reverse transcriptase-polymerase chain reaction approach. RESULTS: Toxicity of human chorionic gonadotropin-doxorubicin conjugates was increased compared with unconjugated doxorubicin in OVCAR-3 cells. However, drug conjugates failed to demonstrate increased toxicity in other cell lines, especially after preincubation with human chorionic gonadotropin. All cell lines expressed luteinizing hormone/human chorionic gonadotropin receptors. Receptor expression in OVCAR-3 cells was not effected by human chorionic gonadotropin, endothelial growth factor, or 8-bromo-cyclic adenosine monophosphate treatment. In other cell lines, receptor expression was down-regulated by these agents. CONCLUSION: Cytotoxic activity of doxorubicin was increased specifically by conjugation to human chorionic gonadotropin. However, the regulation of luteinizing hormone/human chorionic gonadotropin receptor expression and other compounds may reduce the drug-uptake of the conjugates.

Antibiotics, Antineoplastic↗