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PubMed1992

Beta-endrophin immunoreactivity during human pregnancy.

The human placenta has been implicated as a source of numerous peptide hormones during pregnancy. Since the immunoassay detection of the proopiomelanocortin derived peptide beta-endorphin (beta E) in placental extracts in 1978, it has remained uncertain whether placental beta E immunoreactivity (IR) is 1) secreted into the maternal circulation and 2) opiate receptor active during pregnancy. To elucidate the nature of beta E IR in the placenta, both beta E IR and N-alpha-acetylated beta E (Ac beta E) IR were simultaneously measured in extracts of human pituitaries, placentas, and plasma by two homologous RIAs. Pituitary extracts (n = 6) contained 38 +/- 7 nmol beta E IR per g wet wt tissue (mean +/- SEM), of which only 20 +/- 4 pmol/g were Ac beta E IR. Term placental extracts (n = 19) had 201 +/- 30 fmol/g wet wt total beta E IR and 30 +/- 3 fmol/g wet wt total Ac beta E IR, which comprised 15% of total beta E IR in placental extracts. Total plasma beta E IR rose from 28 weeks gestation (8.5 +/- 0.3 fmol/mL, n = 159) to peak at labor (50 +/- 4 fmol/mL, n = 98; P < 0.01) but total Ac beta E IR was found in only four 28-week (1.7 +/- 0.9 fmol/mL) and 42 labor plasma samples (0.9 +/- 0.1 fmol/mL). Gel filtration chromatography of placental and pituitary extracts showed that while less than 1% of the beta E31-size material was acetylated in the pituitary, up to 60% of the beta E31-size material in placental extracts was acetylated. In pooled third trimester plasma extracts, however, only 4% of the beta E31-size material was acetylated. Furthermore, the ratio of beta E31:beta-lipotropin in pituitary extracts (n = 3) was 0.5; pooled plasma-0.5, and placental extracts (n = 5)-1.2. These data indicate that 1) the placenta extensively N-alpha-acetylates beta E31 destroying its opiate bioactivity while the pituitary does not; 2) beta E IR in pregnant women's plasma is similar to pituitary beta E IR, being mostly nonacetylated and similar in size to beta-lipotropin. These findings are consistent with a pituitary source for the elevated plasma beta E IR found during late pregnancy which may, in turn, be a consequence of elevated plasma concentrations of placentally secreted plasma corticotropin-releasing factor IR present during the third trimester.

Acetylation↗

PubMedDate not supplied

Oral submucous fibrosis in a 12-year-old girl: case report.

A case of oral submucous fibrosis in a 12-year-old girl discusses its etiopathogenesis, clinical features, and histopathologic findings of the condition and highlights strong association of areca nut chewing as the potential factor in the etiology of this condition. Cessation of the areca nut chewing habit and submucosal administration of aqueous extract of healthy human placental extract (Placentrex) showed marked improvement of the condition. (Pediatr Dent 15:120-22, 1993).

Areca↗

PubMedDate not supplied

Inhibitors of platelet aggregation in the fetoplacental unit and myometrium with particular reference to the ADP-degrading property of placenta.

Extracts of fresh tissue from the feto-placental unit and myometrium were tested for their ability to inhibit ADP-induced platelet aggregation and to degrade ADP. Placental extracts caused rapid reversal of aggregation and degraded ADP, both effects being mimicked by HPAP. However, whereas the latter was inhibited by L-phenylalanine but not by heating to 65 degrees C for 5 minutes, the reverse was true for crude placental extracts. Umbilical cord vessels and myometrium totally inhibited platelet aggregation in a similar way to pure PGI2. Both tissues also exhibited ADP-ase activity but were much less potent in this respect than placenta. In the system used, little or no anti-aggregatory activity was detected in extracts of non-vascular cord tissue, fetal membranes or amniotic fluid, although the two latter tissues had a weak ADP-degrading effect. Thus, it appears that in contrast to myometrium and umbilical cord vessels, the major inhibitor of platelet aggregation in placenta is an ADP-ase and not PGI2. While part of the inhibitory effect of placenta may be due to HPAP, other ADP-degrading enzymes also seem to contribute to the overall anti-aggregatory property of this organ.

Alkaline Phosphatase↗

PubMed1976

Identification of a butanol-extractable human placenta-specific antigen with alkaline phosphatase activity.

N-Butanol extracts of whole-term placenta from different individuals were prepared, and used as immunogens to raise heterologous hyperimmune sera in rabbits. Upon immunoelectrophoresis the anti-placenta antisera could recognize at least six antigenic components in the placental extract even after they had been completely absorbed with pooled male serum proteins. However, the antisera so absorbed, designated (-PMS) antisera, could still react strongly with several normal adult tissue extracts including kidney. Systematic and quantitative absorptions of the (-PMS) antisera were thus further carried out with individual butanol extracts of normal adult liver, lung, intestine, stomach, kidney, bone, pancreas, spleen, heart, cerebrum, cerebellum, breast, and packed red cells, as well as a composite extract containing equal amounts of each of the 13 adult tissue extracts. Of the six antigenic components in the placental extracts reacting with the (-PMS) antisera the only one which retained its reactivity with the antisera throughout exhaustive absorptions was associated with alkaline phosphatase activity. This immunologic and enzymologic identity was confirmed with homogeneous placental alkaline phosphatase. Extracts from each of three placentae injected into three pairs of rabbits all produced an identical antibody reaction with the unique determinant(s) of placental alkaline phosphatase. The same identity of precipitin reaction was also found with extracts of 14 other placentae against each of these antisera. It thus firmly establishes that placental alkaline phosphatase is a characteristic placenta-specific fetal protein.

Absorption↗

PubMed1991

The effect of horse placental tissue extracts and equine chorionic gonadotrophin on the proliferation of horse lymphocytes stimulated in vitro.

Commercial preparations of equine chorionic gonadotrophin (eCG) and extracts of horse placenta taken at 80 days gestation were incorporated into mixed lymphocyte culture and mitogen stimulation assays of horse peripheral blood mononuclear cells. A dose-related inhibition of lymphocyte proliferation, indicative of immunosuppressive activity, was observed in both systems, both with commercial eCG preparations and tissue extracts. Negligible inhibitory activity was observed with an extract of term placenta. The inhibitory activity of the placental samples was not related to their eCG content as measured by immunoassay. The fact that one pregnant horn allantochorion extract containing 50 IU/ml of eCG showed an identical dose-dependent lymphoproliferation-inhibitory activity to an extract of a second such allantochorion containing only 1.7 IU/ml of eCG suggests that this hormone does not inhibit lymphocyte proliferation and that commercially available eCG contains inhibitory contaminants.

Animals↗

PubMed1990

Placental transfer of glucose and amino acids in intrauterine growth retardation: studies with substrate analogs in the awake guinea pig.

After experimentally inducing growth retardation by unilateral uterine artery ligation in midpregnancy, placental blood flow (PBF) (microsphere technique) and placental transfer of 14C-aminoisobutyric acid (AIB) and 3H-methylglucose (MG) were studied at d 44, 50, or 63 of gestation in 19 chronically catheterized awake guinea pigs. At d 44, fetal wt (FW) and placental wt were reduced by 16 and 18%, respectively, in the ligated horn and FW/PBF was increased by 122%. Placental efficiency to transfer MG and AIB (fetal dpm/g placenta) was maintained in the ligated horn, feto-placental extraction (feto-placental dpm/PBF) was increased, and placental transfer of the substrate analogs (fetal dpm/g fetus) was unchanged. At d 50 and 63, placental wt and FW were reduced in proportion (approximately 40%) in the growth-retarded group and FW/PBF was increased by 80 and 51%, respectively. Placental transfer of AIB was reduced by 33% at d 50 and by 18% at d 63. In addition, placental efficiency to transfer AIB was reduced by 36% at d 50 and by 22% at d 63 in the growth-retarded group. Fetal uptake of MG per g fetus was slightly reduced (-6%) at d 50 of gestation, but unaffected at d 63. Extraction of MG from the maternal PBF was increased, whereas the wt-specific transfer capacity of the placenta was unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)

3-O-Methylglucose↗

PubMed1978

Characterization of relaxin radioimmunoassay using Bolton-Hunter reagent. First results in plasma during pregnancy, and in placenta, corpora lutea and ovarian cysts in woman.

Application of a porcine relaxin radioimmunoassay system using Bolton and Hunter reagent was characterized in different biological fluids. In pregnant woman, plasma reveals concentrations from undetectable values to 1,800 pg/ml. Maximal concentrations are found between the 8th and the 13th weeks of pregnancy. These peak values are significantly different from those at other stages of pregnancy. Appreciable relaxin concentrations are detected in gestational corpus luteum extract, and in corpora lutea cyst fluid of pregnant and nonpregnant women. No relaxin was detected in a cyclus corpus luteum extract, in a placental extract, or in an ovarian serous cyst. The presence of immunoreactive relaxin in the nonpregnant woman is reported.

Female↗

PubMed2002

Detection of human kallikrein 4 in healthy and cancerous prostatic tissues by immunofluorometry and immunohistochemistry.

BACKGROUND: Human kallikrein 4 (gene, KLK4; protein, hK4), a recently discovered member of the kallikrein gene family, shares many characteristics with prostate-specific antigen, the best available marker for prostate cancer. Because the protein has not been detected in any human tissue, we attempted to develop immunologic methods for hK4 analysis and use them to detect hK4 in healthy and cancerous tissue extracts and biological fluids. METHODS: We extracted total RNA from 20 pairs of matched (healthy-cancer) prostate tissue samples. KLK4 cDNA was amplified by reverse transcription-PCR (RT-PCR) and cloned in a pPICZalphaA expression vector. We then transformed the construct product into Pichia pastoris yeast strains and induced secreted recombinant protein production by addition of methanol. We purified the recombinant protein by nickel ion-affinity chromatography and used it as an immunogen in rabbits and mice to generate polyclonal anti-hK4 antibodies. These antibodies were used to develop a sandwich-type immunoassay suitable for hK4 quantification in biological fluids and tissue extracts. RESULTS: The immunoassay had a detection limit of 0.1 microg/L. We detected hK4 in 10 of 21 matched (healthy-cancer) prostate tissues, and hK4 was frequently higher in healthy tissues. In one matched-sample pair, the hK4 content was relatively high in both the healthy [4.62 microg/g of total protein (TP)] and the cancerous (1.22 microg/g of TP) prostate tissue. Among tissue extracts, we found the highest concentrations of hK4 in healthy (0.0-4.62 microg/g of TP) and cancerous (0.0-1.72 microg/g of TP) prostatic extracts and in placental extracts (0.0-0.05 microg/g of TP). We also detected traces of hK4 protein immunoreactivity in amniotic fluid (<0.1-0.6 microg/L), human breast milk (<0.1-0.75 microg/L), and seminal plasma (0.2-0.9 microg/L). Immunohistochemical studies showed cytoplasmic staining for hK4 protein in both malignant and benign epithelial cells of the prostate. However, we did not detect hK4 in cerebrospinal fluid, healthy and cancerous ovarian tissue extracts, and many other human tissue extracts. CONCLUSIONS: hK4 protein is present in some prostatic tissue extracts but at relatively low concentrations, although KLK4 mRNA is readily detectable by RT-PCR. We propose that the protein either is not synthesized efficiently or is degraded very quickly.

Animals↗

PubMed1989

[Primary screening of the immunopharmacologic activity of Filatov tissue therapy preparations].

The paper presents results of primary assessment of immunopharmacologic activity of tissue preparations (peloidodistillate, FiBS, torfot, extract of aloe, placental extract) and the study of their influence on basic links of immune response (experimental investigations were carried out with mice-hybrids F1). It is found that the studied bioregulators possess immunomodulating action on primary humoral immune response and don't increase a hypersensitive reaction of a slowed type. The direction of immunotropic action of tissue preparations depends on the state of immunologic reactivity of the body and the kind of a preparation (variety of immunopharmacologic activity of the distillates groups and albumin preparations). It is expedient to work out indications to the usage of tissue preparations after V. P. Filatov to prevent and treat immunodeficient and immunopathologic conditions of the body.

Animals↗

PubMed1984

[Determination of the concentration of chorionic gonadotropin (HCG) and its free subunits in placental tissue during various periods of normal pregnancy].

The aim of this study was to estimate HCG and its free subunits (alpha and beta) content in placental tissue and to determine the characteristic pattern of their ratio changes in the course of normal pregnancy. For this we used 47 samples of placental extracts. The tissue was extracted and gel filtrated on a calibrated Sephadex-G-100 column. Crude placental extracts and each fraction after chromatography were radioimmunoassayed for HCG, alpha HCG and beta HCG in a double antibody, homologous radioimmunoassay system. We obtained the following results: Peak of native HCG secretion occurred in 6-8 gestational week thereafter its concentration in placenta decreases. The absolute amount of free alpha HCG increased after the first trimester like to native HCG, but the relative quantity of alpha HCG exceeded that for HCG. In extracts from mature placenta quantity of free alpha HCG was about 5-10-fold more than HCG. In chorionic extracts from the first trimester we have proved the free beta subunit of HCG. It has not been found in extracts from mature placenta.

Chorionic Gonadotropin↗

PubMed1993

Growth of only highly tumorigenic cell lines is inhibited by EAP, a human placental fraction.

We have previously shown that a fraction from a human placental extract, EAP, inhibited growth in soft agar of a human lung squamous adenocarcinoma cell line, A-2182, and of Ha-ras oncogene-transfected murine BALB/c 3T3 cells. We report here the activities of this extract on several cell lines which have different degrees of transformed phenotype. Human esophagus and colorectal cell lines were derived from tumors at different stages of neoplasic progression, and murine BALB/c 3T3 cells were transfected with various oncogenes. In all three models, growth of the most highly tumorigenic cells was inhibited by the presence of EAP in soft agar medium, while growth of non- and low tumorigenic counterparts was not affected or was stimulated by the placental extract. In addition, EAP did not significantly affect the doubling time of anchorage-dependent cell growth, suggesting that EAP specifically suppresses tumorigenic characteristics of cells such as their ability to grow in soft agar medium. These effects appear to be in contrast to those of transforming growth factor beta, which exerts its most profound effect on less tumorigenic cells.

3T3 Cells↗

PubMed2000

Processing of procorticotropin-releasing hormone (pro-CRH): molecular forms of CRH in normal and preeclamptic pregnancy.

This study examined the different molecular forms of CRH in normal and preeclampsia maternal plasma and protease-blocked placental extracts using antibodies to different regions of the CRH precursor, pro-CRH. In the absence of protease inhibitors, chromatographed normal placental extracts contained four peaks of immunoreactivity corresponding to unprocessed approximately 19-kDa pro-CRH, its approximately 8-kDa intermediate metabolite, pro-CRH125-194, its approximately 2.8-kDa midportion fragment, pro-CRH125-151, and 4.75-kDa CRH1-41. However, if protease inhibitors were included in the extraction medium, only pro-CRH and pro-CRH125-194 were found. Pro-CRH processing was more extensive in protease-blocked preeclampsia placentas than in those from normal pregnancy, with three peaks corresponding to pro-CRH, proCRH125-194, and mature CRH1-41 peptide found. Using quantitative competitive PCR, the messenger ribonucleic acid levels of CRH precursor in preeclampsia placentas were 1.7-fold higher than those in normal placentas (37.83 +/- 3.48 vs. 21.83 +/- 2.59 attomoles/microg total ribonucleic acid, respectively; P < 0.005). Preeclampsia placentas contained significantly more CRH1-41 cross-reactivity (4.72 +/- 1.22 pmol/g) than normal term placentas (1.52 +/- 0.39 pmol/g; P < 0.048) extracted in medium containing protease inhibitors. The content of pro-CRH(125+/-151)-reactive species in these extracts followed the same pattern, with more immunoreactivity detected in preeclampsia placentas (4.23 +/- 1.39 pmol/g) than in those from normal term pregnancies (1.44 +/- 0.32 pmol/g; P < 0.01). Sequential plasma samples from 10 women with normal pregnancy and 5 women with preeclampsia were assayed for pro-CRH(125-151)- and CRH(1-41)-immunoreactive species In normal pregnancy, maternal plasma CRH(1-41) immunoreactivity rose with increasing gestational age, reaching 460 +/- 48 pmol/L at term. In women with preeclampsia, CRH(1-41) levels at each gestational age point were higher than those at the equivalent stage of normal pregnancy. In contrast, the levels of pro-CRH(125-151)-immunoreactive species remained barely detectable throughout normal and preeclamptic pregnancy. Both pro-CRH and CRH(1-41), but not pro-CRH(125-151), were shown to bind to the plasma CRH-binding protein. Our findings highlight the importance of protection of placental tissue from degrading enzymes during extraction and show that most of the CRH in the human placenta exists as unprocessed pro-CRH, with very little in the form of CRH(1-41) except in preeclampsia. Our studies using maternal plasma indicate that CRH(1-41) is the only one of the pro-CRH fragments studied to be maintained in significant amounts in the maternal circulation and also the only fragment studied for which a specific plasma binding protein exists.

Animals↗

PubMed1996

Specificity of a placental factor inhibiting breathing in fetal sheep.

We have found previously that the infusion of a placental extract inhibits breathing induced by 100% O2 plus umbilical cord occlusion in the fetal sheep, suggesting that a placental factor is responsible for the inhibition of fetal breathing. To test whether this factor is specific to the placenta and whether it also inhibits spontaneous fetal breathing (occurring in the absence of cord occlusion), we administered extracts from the placenta, muscle and liver of the pregnant ewe, extracts of fetal liver, and Krebs solution to 16 chronically instrumented fetal sheep at 135 +/- 5 days of gestation. Infusions were made during low-voltage electrocortical activity, 5 to 15 min after a switch from high voltage, when breathing was well established. Within 90 s of the infusion of the placental extract in the carotid artery of the fetus, breathing decreased in 79% (33/42) of the experiments and was completely abolished in 71% (30/42) of them (P < 0.0001 compared with the other infusates). No apnoeas were observed with the Krebs solution (0/19) and the maternal muscle (0/20). Extracts of maternal and fetal liver abolished breathing in only 17% (4/23) and 21% (6/29) of the experiments respectively (NS compared with Krebs solution). There were no significant changes in blood gas tensions, pH, blood pressure and heart rate associated with the infusion of the extracts. The electrocortical activity (ECoG) switched from low to high voltage in 50% of the experiments using placental extract compared with 0% with Krebs solution and maternal muscle, and with 9% and 17% with maternal and fetal liver respectively (P < 0.005). Breathing output (integral of EMGdi x f) during and after the infusions significantly decreased only with the placental extract. These findings indicate the presence of a factor produced by the placenta which inhibits fetal breathing and may be responsible for the normal inhibition of breathing observed in fetal life.

Animals↗

PubMed1990

Merosin, a tissue-specific basement membrane protein, is a laminin-like protein.

Merosin is a basement membrane-associated protein found in placenta, striated muscle, and peripheral nerve. A 3.6-kilobase merosin cDNA clone was isolated from a placental cDNA expression library. The clone contained a 3.4-kilobase open reading frame, the 3' portion of which includes protein sequences of proteolytic fragments of merosin. The deduced amino acid sequence of the merosin polypeptide was similar to that of the COOH-terminal region of the 400-kDa A chain of laminin. This part of laminin forms the large globule at the end of the long arm of the laminin cross and is thought to contain the neurite-promoting site and the major cell binding site(s) in laminin. The sequence identity between merosin and the laminin A chain in this region is nearly 40%. An antiserum against a synthetic peptide from the middle of the merosin cDNA sequence identified a 300-kDa polypeptide in placental extracts, indicating that the merosin polypeptide is similar in size to the laminin A chain. Intact merosin was isolated from placental extracts and shown to be covalently associated with the laminin B chains and to have a cross-like structure similar to that of laminin. The similarities between merosin and laminin show that both proteins are members of the same family of basement membrane proteins.

Amino Acid Sequence↗

PubMed1982

Endogenous inhibition of prolactin secretion in pregnant lactating rats.

The purpose of the present study was to test whether rat placental lactogen, proposed to be inhibitory for endogenous rhythmic PRL secretion during pregnancy, is also inhibitory for a neurally mediated PRL response to exogenous stimulation, i.e. suckling. Pregnant lactating rats were used as the model in this study. Blood samples for PRL were taken via a chronic atrial cannula before and after 30 min of suckling stimulation in the following groups of females: 1) bearing conceptuses of different degrees of development; 2) after removal of conceptuses; and 3) after injection of placental extract immediately before exposure to suckling stimulation. It was found that 1) the PRL response to suckling diminished in conjunction with placental development and the known concomitant rise in rat placental lactogen; 2) removal of the conceptuses permits elevation of PRL after suckling stimulation; and 3) injection of placental extract obtained on days 11-12 of pregnancy failed to block the elevation of PRL in response to suckling. It was concluded that 1) lactation can be maintained even in the presence of very low levels of PRL, provided developed placentae are present, and 2) the developed placentae are capable of inhibiting the acute PRL release in response to exogenous stimulation as well as endogenous rhythmic PRL secretion.

Animals↗

PubMed1990

Expression and localization of growth hormone-releasing hormone messenger ribonucleic acid in rat placenta: in vitro secretion and regulation of its peptide product.

The placenta is the source of many hypothalamic peptides. We now report that GH-releasing hormone (GHRH) mRNA was detectable in rat placenta. On Northern blot hybridization analysis, the size of the placental GHRH transcript was the same with the putative GHRH precursor mRNA. On in situ hybridization, the cells expressing the GHRH mRNA had the morphological characteristics of cytotrophoblasts. In addition, immunoreactive (IR) postranslational products of GHRH were present in rat placental extracts and in the effluent of in vitro perifused placentae. On gel filtration chromatography, the bulk of IR-GHRH present in placental extracts and perifusion effluent had the same size as the authentic hypothalamic GHRH (5.2K). A higher mol wt form of IR-GHRH of about 10K was also present and may represent the pro-GHRH predicted from the sequence of the GHRH cDNA. The mean basal release of IR-GHRH in the perifusion effluent from full thickness rat placental fragments was 337.3 +/- 38.5 (+/- SE; n = 48) pg/10 min fraction.g tissue. Depolarization by 56 mM KCl increased the concentration of the secreted immunoreactive peptide to 632.2 +/- 50.5. A 10-min exposure to 8-bromo-cAMP caused an immediate, monophasic, and dose-dependent increase in IR-GHRH secretion, which lasted between 20-30 min. The ensuing response to a KCl pulse was similar in size and pattern to that in the control channels. In contrast, a 10-min pulse of phorbol 12-myristate 13-acetate (a protein kinase-C-irreversible activator) induced a gradual, prolonged, and dose-dependent increase in basal GHRH secretion which lasted for at least 4 h. Additionally, phorbol 12-myristate 13-acetate enhanced KCl-induced GHRH secretion. In conclusion, our data suggest that the GHRH gene is expressed in the rat placenta. The placental GHRH transcript and its peptide products appear to have the same size as their hypothalamic counterparts, while the site of its placental GHRH synthesis is the cytotrophoblast. Finally, the secretion of placental GHRH seems to be regulated by both the adenyl cyclase and the protein kinase-C pathways.

Animals↗

PubMedDate not supplied

Placental and maternal serum inhibin-A and activin-A levels in Down's syndrome pregnancies.

The objective of this study was to analyse the levels of inhibin-A and activin-A in maternal serum and placental tissue from Down's syndrome (DS) pregnancies. Inhibin-A and activin-A levels were determined by specific immunoassays and individual results were expressed as multiples of the control median (MoM) at the appropriate gestation. Immunohistochemistry was used to localize inhibin alpha and beta(A)-subunits in a selection of placental sections. In DS pregnancies, median inhibin-A levels were found to be significantly elevated to 1.46 MoM (P< 0.05) in placental extracts, and 2.06 MoM (P< 0.0001) in maternal serum, when compared with uncomplicated pregnancies. Median activin-A MoMs were also elevated in placental extracts and maternal serum to 1.62 MoM (P< 0.01), and 1.26 MoM (P< 0.05), respectively. Immunohistochemistry revealed that the alpha subunit of inhibin-A and the beta(A)subunit of inhibin-A and activin-A were mainly localized to the trophoblastic layer of placental villi. Semiquantitative studies of staining intensity revealed a trend towards stronger staining of placental trophoblasts and stroma of DS tissues, although this was statistically significant only for beta(A)subunit staining of trophoblasts (P< 0.05). These results support the hypothesis that maternal serum levels of inhibin-A and activin-A are elevated due to increased production in the placenta, and increased immunostaining of trophoblasts suggests that this may be due to increased production in the trophoblasts.

Activins↗

PubMed1991

The neuropeptide, head activator, in human placenta and serum from pregnant women.

The hydra neuropeptide, head activator, was detected in human placenta using radioimmunoassay. The placenta contained 11-68 fmol/g wet weight of head activator. The slope of the inhibition curve by placental extract in radioimmunoassay was identical to that of synthetic head activator. The molecular weight of the major immunoreactive head activator in placental extract corresponded to the synthetic head activator after Bio-Gel P-2 column chromatography. The peak of immunoreactive head activator in the extract emerged at the same retention time as that of the synthetic head activator on reversed-phase high-performance liquid chromatography. Head activator was localized histologically in trophoblasts of placenta by peroxidase-antiperoxidase staining techniques. The head activator staining was inhibited by the excessive synthetic head activator. The serum head activator level during pregnancy ranged from 9 to 31 pmol/l. A positive linear correlation was found between serum head activator content and gestational weeks.

Amino Acid Sequence↗