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At least 91 records · Page 5Linked to original sources
PubMed1986

Studies of monoclonal antibodies against human chorionic gonadotropin. II. Applications of human chorionic gonadotropin monoclonal antibodies on immunoassays.

Monoclonal antibodies generated against human chorionic gonadotropin (hCG) were utilized in radio- and enzyme-immunoassays of this reproductive hormone in biological fluids. One of the monoclonal antibodies, beta-4D6, was shown to have extremely high affinity (Ka = 8 X 10(10) M-1)) and high specificity (less than or equal to 0.6% LH cross-reactivity) to beta-subunit of hCG and whole hCG. It was used in competitive radioimmunoassays (RIA) for the determination of low levels of serum hCG. An excellent correlation was obtained concerning the assay results between the monoclonal antibody-based system and others using conventional polyclonal anti-sera. In combination with another discrete hCG monoclonal antibody, solid-phase sandwich radiometric and enzyme immunoassays were established. These immunoassays could easily be performed, and they offer sensitivity and efficacy of hCG determination comparable to those of conventional ones.

Animals↗
PubMed1984

Mechanism of induction of human chorionic gonadotropin in lung tumor cells in culture. Increased levels of alpha-human chorionic gonadotropin-specific mRNA sequences and benzo(a)pyrene-induced hypomethylation.

Human lung cells (ChaGo) derived from a bronchogenic carcinoma produce human chorionic gonadotropin (hCG), predominantly the alpha subunit of the glycoprotein hormone, under culture conditions. Treatment of the cells with the polycyclic aromatic hydrocarbons, benzo(a)pyrene (BaP) or dimethylbenzanthracene, at concentrations which do not affect cell growth or macromolecular synthesis, stimulates the production of hCG in these cells. The levels of alpha hCG-specific mRNA (mRNA alpha hCG) sequences in total poly(A)+ RNA isolated from control and drug-treated ChaGo cells are determined by the dot hybridization technique using 32P-labeled, cloned cDNA alpha hCG probe. A concentration-dependent increase in the levels of mRNA alpha hCG sequences in BaP or dimethylbenzanthracene-treated ChaGo cells has been observed. The increase in the level of mRNA alpha hCG sequences can be detected after treatment of the cells with either of the drugs for 24 h, and this level attains its maximum within 48-72 h following drug treatment. A comparative study of the restriction endonuclease (MspI/HpaII) digestion patterns of the control and BaP-treated cell DNA suggests that the internal "C" residues of the -CCGG- sequences in the alpha hCG gene of untreated cells are highly methylated; whereas the internal C residues of the same MspI/HpaII recognition sequences in the alpha hCG gene are comparatively less methylated in BaP-treated cell DNA.

Benzo(a)pyrene↗
PubMed1983

Plasma human chorionic somatomammotropin deficiency in a normal pregnancy is the consequence of low concentration of messenger RNA coding for human chorionic somatomammotropin.

Human chorionic somatomammotropin (hCS) is important in the hormonal monitoring of human pregnancies. Presented is the case of a clinically normal pregnancy in which a very low plasma level of hCS was detected. The concentration of messenger ribonucleic acid (mRNA) coding for hCS was evaluated to determine the level on which the deficiency occurred.

Adult↗
PubMed1996

"Repair' of the chorionic somatomammotropin-A "enhancer' region reveals a novel functional element in the chorionic somatomammotropin-B enhancer.

Human chorionic somatomammotropin (CS) synthesis results from the independent expression of two homologous genes, CS-A and CS-B. A transcription enhancer factor-1 (TEF-1) element and an upstream 81 bp modulatory domain, containing repressor (RF-1) and derepressor (DF-1) activities, are important for efficient CS-B enhancer function in transfected placental JEG-3 cells. The equivalent region of the CS-A gene is not active. Although the TEF-1 element is conserved between the CS-A and CS-B genes, a single base substitution is present in the DF-1 element and two more are located between the RF-1 and DF-1 sites in a region we term AF-1. Repair of the DF-1 site increased CS-A enhancer function approximately 70-fold, but repair of previously uncharacterized AF-1 sequences was also required for full (CS-B like) enhancer activity. A 5 bp disruption of AF-1 sequences in the CS-B enhancer region, resulted in a 97% loss of stimulatory activity. The AF-1 sequences showed no intrinsic enhancer activity, however, they were able to significantly repress heterologous promoter activity stimulated by a TEF-1 enhancer element. A high affinity/specificity interaction between JEG-3 nuclear protein and AF-1 sequences was confirmed by gel mobility shift assay. By comparison to "wild type' AF-1 sequences, this interaction was competed to a lesser extent by both RF-1 and DF-1 elements, but not by mutated AF-1 sequences. The major protein binding to AF-1 sequences was estimated to be 23 kDa by UV crosslinking. These data indicate that enhancer activity can be generated by modulating binding events proximal to the TEF-1 element in the CS-A "enhancer' region and that coordinated binding of AF-1 and DF-1 are required for efficient (CS-B) enhancer activity.

Base Sequence↗
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↗
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↗