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PubMed1987

Clinical experience with the use of peripheral vasodilator in oral disorders.

Conventional therapies practised in the treatment of asymptomatic neuralgia, oral submucous fibrosis and paraesthesic numbness, are empirical and symptomatic in nature. These are usually prolonged and may be inadequate, impractical with complete or incomplete remissions associated with or without relapses. High dosages of drugs administered for longer duration, are also not infrequently without side-effects. With these problems in view, the clinical use of nylidrin hydrochloride a peripheral vasodilator, was experienced for over 10 years. Irrespective of age, sex and status, 97 cases were randomly extracted from the hospital and oral surgery clinical records. The projected sample included 33 cases of asymptomatic neuralgia, 58 cases of oral submucous fibrosis and 6 cases of numbness. Neuralgia, where mean age was 50 years, was treated with nylidrin hydrochloride, vitamin B-complex and carbamazepine. Oral submucous fibrosis where mean age was 38 years, was treated with nylidrin hydrochloride, vitamins A,E,B-complex, iodine, placental extract, local and systemic corticosteroids and physiotherapy. Paraesthesic numbness, following iatrogenic or accidental trauma to the affected nerve, was treated with nylidrin hydrochloride and B-complex therapy. Peripheral vasodilator administered in all 97 cases, initially contained low divided doses, which steadily were increased or decreased as per individual response. There were reportedly no side-effects, except complaints of flushingly warm skin. Supportive therapy with antibacterials, tranquilizers and analgesics, along with minor dental surgery, were given as and when required. The success rate was 72.16% in total, while individually it varied from 84.85% in neuralgia, 62.07% in oral submucous fibrosis and 100% in numbness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1977

Lactogenic activity in the serum of rabbits during pregnancy and early lactation.

The levels of lactogenic activity in the serum of rabbits during pregnancy and early lactation have been determined. The accuracy and sensitivity of the radioreceptor assay used were increased by several technical improvements. Lactogenic activity remained low throughout pregnancy and increased at parturition; the highest values were reached on day 5 of lactation. No lactogenic activity was detected in placental extracts of rabbits, suggesting that the lactogenic activity measured in the serum is solely of pituitary origin. These results are discussed in relation to the main stages of development of rabbit mammary glands.

Animals↗
PubMed1997

Detection of novel molecules recognized by anti-placental lactogen antibody in rat amniotic fluid.

Amniotic fluid contains various bioactive substances including the placental PRL family. In the present study, it was elucidated that rat amniotic fluid contained immunoreactive proteins which had different molecular sizes and pI values from the authentic placental lactogens (PLs) in the rat, recognized by antipeptide antibody to the N-terminal peptide of rat PL-I. Immunoreactive PLs residing in the amniotic fluid were characterized further by two-dimensional sodium dodecyl sulfate gel electrophoresis (2DE), immunoblotting and anion-exchange chromatography. Amniotic fluid collected from rats on day 12 of pregnancy contained two PL-like molecules, tentatively called A1 (MW 75 kDa, pI 4.6) and A2 (MW 99-102 kDa, pI 5.3-5.4). A1 and A2 are specific to the amniotic fluid, because no such molecules were found in the serum or placental extracts. Immunoblot analysis of amniotic fluid revealed that A1 levels increased, whereas those of A2 decreased to an undetectable level up to day 16 of pregnancy. When the A1 concentrations from days 12 to 20 were monitored intensively, they increased from day 12 to 14, were maintained until day 18, and then decreased dramatically by day 20. The expression pattern for A1 was therefore completely different from those of authentic placental PRL family members found in serum and placental tissue, indicating that the A1 is distinct from them. Partial purification by anion-exchange chromatography and 2DE revealed that A1 consisted of 5 isoforms.

Amniotic Fluid↗
PubMedDate not supplied

Cysteine proteinase inhibitors in human placenta.

When human placental extract was chromatographed on a Sephadex G-75 column, cysteine proteinase inhibitors with molecular weights of 80 000 and 12 300 were eluted. The high molecular weight peak (CPI-H) was identified as alpha-cysteine proteinase inhibitor. The thermostable low molecular weight peak (CPI-L) inhibited plant proteinases (papain, ficin and bromelain) as well as cathepsins B, H and L isolated from the human placenta. No cross-reactivity was observed between placental CPI-L and serum alpha-CPI.

Antibodies↗
PubMed1995

Nitric oxide synthase in human placenta and umbilical cord from normal, intrauterine growth-retarded and pre-eclamptic pregnancies.

1. It has been suggested that a deficiency of nitric oxide (NO) may explain many of the pathophysiological features of pre-eclampsia (PE) and intra-uterine (foetal) growth retardation (IUGR). To elucidate further the role of NO in the pathophysiology of pregnancy we have determined the relative amount and activity of NO synthase (NOS) in first trimester and normal-term placental tissues, as well as in the placenta and umbilical cord in pregnancies complicated by PE and IUGR, using NG-nitro-L-[2,3,4,5(-3)H]-arginine ([3H]-L-NOARG) binding, quantitative in vitro autoradiography, [3H]-arginine to [3H]-citrulline conversion and Western blotting. 2. Specific, high affinity (KD = 38 nM) [3H]-L-NOARG binding was demonstrated in the villous trophoblast of normal-term placentae. Binding was calcium-independent, stereoselective and exhibited a rank order of inhibition by NOS inhibitors and substrate (L-NOARG > or = L-NMMA > or = 7-NI > L-NAME > L-Arg > or = L-NIO > ADMA). 3. [3H]-L-NOARG binding density and NOS activity were both significantly greater in placental tissues from first trimester and PE or IUGR complicated pregnancies compared to normal-term placentae. 4. Western blotting, using an endothelial NOS peptide antiserum, demonstrated a approximately 140 KDa protein band in placental extracts and indicated that the amount of immunoreactive material was significantly greater in first trimester compared to normal-term placentae. 5. Specific [3H]-L-NOARG binding was also localized to the endothelial lining of umbilical arteries and veins, binding density being greater in the artery than the vein. [3H]-L-NOARG binding to the umbilical artery endothelium was significantly lower in PE and IUGR complicated pregnancies compared to normal-term controls. 6. The role of trophoblast-derived NO in human placental pathophysiology remains to be established, but differences in the amount of placental [3H]-L-NOARG binding, NOS activity and immunoreactive material indicate that expression of NOS in the villous trophoblast falls during pregnancy. Conversely, the apparent reduction in NOS in the umbilical artery endothelium in PE and IUGR complicated pregnancies may be indicative of endothelial dysfunction.

Adult↗
PubMed1991

Biological and immunoactive substances resembling chorionic gonadotropin are present in full-term horse and zebra placentas.

This study describes the presence of immunoactive and bioactive eCG-like material in full-term placentas of both domestic horses and zebras. Term placental extracts were immunoreactive in an LH monoclonal antibody RIA, and methods successfully used previously for the purification of eCG and eLH were employed to further concentrate the immunoreactive materials to the point where additional characterization studies could be performed. Sufficient equine material was obtained to perform a final fractionation on a concanavalin A Sepharose column yielding an unadsorbed fraction, e17A, and an adsorbed fraction, e17B. There was insufficient zebra material, z5D, for this step. HPLC gel filtration coupled with LH immunoassays of the column eluates showed all the final placental fractions to be highly heterogeneous, but a discrete peak of immunoactivity was found in one of the two equine fractions (e17B) and in the zebra fraction (z5D). The HPLC gel filtration elution volumes for e17B and z5D suggest that they have a smaller molecular size than either eCG or eLH but almost the same size as ovine LH. Both e17B and z5D were bioactive in the rat Leydig cell assay for LH but low in potency compared to eCG or eLH; e17A was inactive at very high doses (5 micrograms). This latter fraction, however, cross-reacted in an eCG alpha RIA to a much greater extent (6 times) than e17B, suggesting that it may be an incompletely formed or degraded alpha subunit. RIAs for LH, eCG, and eCG beta suggest that epitopes distinctive for these molecules are also present or similar to those in the term placental materials.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

[Polymorphism in alkaline phosphatase (author's transl)].

1. In horizontal starch-gel electrophoresis placental extracts show an alkaline phosphatase polymorphism which - according to ROBSON and HARRIS - depends on the fetal genotype. Investigations carried out with a series of 73 placentas revealed 5 of the common 6 phenotypes. Their frequencies were in good accordance with the figures published by the English authors. However, there had been difficulties in typing because of obscrue realizing of the patterns. 2. Although there exists a polymorphism of the heart-stable alkaline phosphatase as observed in 66 serum samples from women at delivery, only four types could be distinguished which, however, could not be related to the placental patterns with any certainty. 3. In all but one of 66 samples of cord serum, investigated simultaneously, a single band only could be observed moving at a slower speed than the serum bands of adult pregnant and non-pregnant persons. This is in conformity with the results of the other investigators. 4. In 18 samples of unheated serum the amount of heat-labile alkaline phosphatase was unimportant and did not alter the features of the heat-stable portion of the enzyme. 5. Contrary to expectations, the alkaline phosphatase polymorphism has no medicolegal relevance.

Alkaline Phosphatase↗
PubMed1990

Isolation of plasminogen activator inhibitor-2 (PAI-2) from human placenta. Evidence for vitronectin/PAI-2 complexes in human placenta extract.

Plasminogen activator inhibitor-2 (PAI-2), found in human placenta and pregnancy plasma, was prepared in a highly purified and functionally active form from human placenta. The purification was achieved by a combination of Rivanol and ammonium sulfate precipitation, followed by chromatography on DEAE Affigel Blue, hydroxylapatite and phenylalanine-Sepharose. PAI-2, which is precipitated by low Rivanol concentrations, can be selectively redissolved from the pellet by increasing the Rivanol concentration in the presence of a reducing agent, i.e. dithiothreitol. The purified protein shows a molecular mass of 45 kDa in SDS PAGE, cross-reacts with monoclonal antibodies against PAI-2 (Mab'PAI-2), and inhibits the amidolytic activity of urokinase-type plasminogen activator (u-PA) towards the chromogenic substrate Glu-Gly-Arg-pNA (S-2444). The specific activity of the purified inhibitor was 52,300 units/mg, attaining 71,000 units/mg in peak fractions. In the immunopurification of placental extract on anti-PAI-2 Sepharose, the eluate showed the expected reaction with Mab' PAI-2, and it also cross-reacted with anti-vitronectin serum. In order to complement these results, anti-vitronectin Sepharose was used for immunopurification of placenta extract. In Western Blot experiments the eluates of anti PAI-2 Sepharose and anti-vitronectin Sepharose both showed a heterogeneous pattern of high molecular weight bands recognized by either polyclonal antiserum against vitronectin or Mab'PAI-2. In either case, reduction of the eluates releases mainly a 45-kDa band, which is recognized by Mab'PAI-2, or 80-kDa and 76-kDa bands recognized by anti-serum against vitronectin. These data suggest that the predominant form of PAI-2 in placenta extract is heterogeneous and of high molecular mass, containing complexes in which vitronectin is covalently bound to PAI-2 by disulfide bridges.

Blotting, Western↗
PubMed1990

Changes in active and latent collagenase in human placenta around the time of parturition.

High levels of collagenase are present in cervical extracts and in the circulation in women at parturition. This study examines the content of collagenase in human placentas at term, the possible contribution to circulating enzyme, and the changes that occur at parturition. Active and latent forms of collagenase are detectable in placentas with apparent relative molecular mass of 60,000 and 65,000 d, respectively. Gel-filtration chromatography was used to identify the presence of excess tissue inhibitor of metalloproteinase as the major collagenase inhibitor in the extracellular matrix of human placentas. After the onset of labor, there was a significant increase in total collagenase activity. Inactivation of the tissue inhibitor of metalloproteinase by reduction of placental extracts with dithiothreitol and alkylation with iodoacetamide resulted in a twelvefold to seventeenfold increase in collagenase activity. Umbilical cord collagenase levels were significantly lower than those in maternal circulation. The possibility of circulating collagenase originating from placenta in labor is discussed.

Chromatography, Gel↗
PubMed2006

Expression and cellular localisation of chloride intracellular channel 3 in human placenta and fetal membranes.

Chloride channels regulate the movement of a major cellular anion and are involved in fundamental processes that are critical for cell viability. Regulation of intracellular chloride is achieved by multiple classes of channel proteins. One class of putative channels are the chloride intracellular channel (CLIC) family. Evidence suggests that several CLICs are expressed in human placenta, although their roles in this tissue are not certain. Northern blot analysis has shown that CLIC3 is highly expressed in placenta relative to other human tissues; however, its cellular distribution is not known. This study used microarray expression profiling to clarify which CLICs are expressed in human placenta and RT-PCR, Western blot and immunohistochemistry to determine the expression pattern of CLIC3 in human placenta and fetal membranes. Placentas and fetal membranes were obtained from term pregnancies after delivery and placental tissue was obtained from first trimester following either chorionic villous sampling or elective pregnancy termination. Trophoblast cells were isolated from first trimester and term placentas and placental endothelial cells were isolated from term placentas. Microarray expression profiling identified high expression of mRNA for CLICs 1, 3 and 4 in the isolated first trimester and term trophoblast cells. High mRNA expression in the isolated endothelial cells was also found for CLICs 1 and 4, but not CLIC3. Low expression was found for CLIC5 in all three types of isolated cells. RT-PCR confirmed that CLIC3 mRNA was expressed in trophoblast cells at both gestational ages, but was not present in endothelial cells. CLIC3 mRNA was also identified in whole placental extracts at both gestational ages and in term amnion and choriodecidua. Immunohistochemistry using a chicken anti-human CLIC3 antibody localised strong CLIC3-specific staining to the syncytiotrophoblast and villous cytotrophoblast cells in both first trimester and term placentas, and weaker staining in extravillous trophoblast cells in first trimester. In fetal membranes at term strong CLIC3-specific staining was localised to chorionic trophoblast cells, with weaker staining in amniotic epithelial and decidual cells. It was previously shown that chloride uptake was increased into cells that had been transfected with CLIC3. CLIC3 may facilitate chloride ion movement and the regulation of cellular processes associated with the movement of chloride in the placental and fetal membrane cells in which it is expressed.

Chloride Channels↗
PubMed1994

Purification and characterization of the constitutive nitric oxide synthase from human placenta.

Human endothelial nitric oxide synthase (NOS) mRNA was detected in human placenta. In contrast, mRNAs for human neuronal NOS or for human inducible NOS were not detected in placenta. Subsequently, NOS was purified over 3800-fold from placental extract to greater than 80% homogeneity. A single band with an apparent molecular weight of 135 kDa was identified by [125I] calmodulin binding to proteins in a sodium dodecyl sulfate-polyacrylamide gel, which is consistent with the predicted size of the endothelial NOS. Furthermore, the sequence of eight internal peptides derived from this 135-kDa protein was identical to the published sequence of human endothelial NOS. As has been shown for all constitutive NOS isozymes, the purified NOS was absolutely dependent on calcium and calmodulin. NOS was also purified from human umbilical vein endothelial cells and, on the basis of similar kinetic parameters and dependence upon calcium and calmodulin, appeared to be the same as the purified placental NOS. Together, these data indicate that the placental NOS is the constitutive NOS isozyme from endothelial tissue.

Amino Acid Oxidoreductases↗
PubMed2000

Increase in 15-hydroxyprostaglandin dehydrogenase activity in the ovine placentome at parturition and effect of oestrogen.

Type 1 NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) is the key enzyme for metabolism of active primary prostaglandins to inactive forms in gestational tissues. The present study examined the activity and immunolocalization of PGDH in the ovine placenta, fetal membranes and uterus over the latter half of pregnancy, and its potential regulation by oestradiol. Placenta, fetal membranes and myometrium were collected from sheep with known single insemination dates on days 70, 100 and 135 of gestation and in active labour demonstrated by electromyographic activity. In addition, chronically catheterized fetuses were infused with oestradiol (100 microgram kg(-1) per 24 h) (n = 5) or saline vehicle into the fetus from day 120 to day 125. PGDH activity measured in placental extracts remained constant from day 70 to day 135 of gestation, and then significantly (P < 0.05) increased by 300% in active labour. Immunoreactive PGDH was localized in the placentome at all stages and was present predominantly in the fetal component of the placentome in uninucleate, but not in binucleate, trophoblast cells. Similarly, in the fetal membranes PGDH immuno-reactivity was present in the uninucleate trophoblast but not in the binucleate cells of the chorion. PGDH immunostaining was also present in the endometrial luminal epithelium, in the smooth muscle of the myometrium, and the glandular epithelium of the cervix. Infusion of oestradiol into the fetal circulation from day 120 to day 125 of gestation had no effect on placental PGDH activity. Immunohistochemistry was used to localize oestrogen receptor alpha in intrauterine tissues to investigate further the failure of oestradiol to increase PGDH activity. Immunoreactive oestrogen receptor alpha was not present in the fetal component of the placenta, although it was expressed in adjacent maternal-derived cells. It is concluded that (1) PGDH activity increases in late gestation; (2) PGDH is expressed in uninucleate trophoblast cells in the ovine placenta and fetal membranes, and also in the maternal endometrial epithelium and stroma, myometrium and cervix; (3) oestrogen receptor alpha is not expressed in fetal cells in the placenta or fetal membranes; and (4) the increase in PGDH activity is not regulated by oestradiol administered to the fetus.

Animals↗
PubMed1983

Heterogeneity of free alpha-subunit in term placenta.

Free alpha-subunit in normal term placenta was examined for molecular weight, electric charge and ability to combine with standard hCG-beta in comparison with extracellular free alpha-subunit and standard hCG-alpha dissociated from urinary hCG in vitro. The gel chromatography on Sephadex G-100 of the placental extract revealed three major immunoreactive hCG-alpha peaks, designated as P alpha-A (Kav = 0.32-0.46), P alpha-B (0.47-0.58) and P alpha-C (0.59-0.70), near the position of standard hCG-alpha. In the isoelectric focusing, while P alpha-A was mainly distributed over the acidic region, the major components of P alpha-B and P alpha-C were distributed over the basic region. Furthermore, in the combination study with standard hCG-beta, such a alpha-subunit with acidic pI scarcely showed any combining activity whereas alpha-subunit with basic pI revealed significant combining activity. These results suggest the following possibilities: that 1) the various size species of placental alpha-subunit may be responsible for the progressive glycosylation; 2) the small alpha-subunit with basic pI may combine with beta-subunit to form immunoreactive hCG; 3) the alpha-subunit, which has not associated with beta-subunit, may be converted to a large and incombinative form with acidic pI by further glycosylation, followed by secretion as a free alpha-subunit.

Chorionic Gonadotropin↗
PubMed1994

The relation between human fetal growth and fetal blood levels of insulin-like growth factors I and II, their binding proteins, and receptors.

OBJECTIVE: To determine the relation between normal human fetal growth and the levels of insulin-like growth factors (IGF-I, IGF-II), their receptors, and IGF binding protein-3 (IGFBP-3) in both the maternal and fetal compartments. METHODS: Serum samples were obtained from normal pregnant women (n = 52) and their fetuses (n = 32) via funipuncture at 21-34 weeks' gestation (mean 29 +/- 4.3) and from term neonates (n = 20) between 38-41 weeks (mean 39 +/- 0.9). Neonates were divided into two groups: the "large" group, whose weights were above the mean for gestational age, and the "small" group, whose weights were below the mean. Aliquots of amniotic fluid (AF) and serum samples were analyzed for levels of IGF-I, IGF-II, and IGFBP-3. Type 1 IGF receptors were assayed from placental extracts of first-trimester elective abortions and from term deliveries. RESULTS: Fetal IGF-I serum levels remained stable throughout most of pregnancy until 34 weeks' gestation (56 +/- 30 ng/mL). Thereafter, IGF-I increased significantly until term (79 +/- 8 ng/mL) (P < .05). Fetal IGF-II levels were relatively unchanged from 23 weeks to term except for a significant increase at 34 weeks. Fetal serum levels of IGFBP-3 averaged 0.8 +/- 0.05 microgram/mL up to 30 weeks' gestation and then increased slightly toward term, at 0.96 +/- 0.05 micrograms/mL. At term, the levels of IGF-I and IGF-II in the AF were not different from the levels in the neonatal serum, but were lower (P < .005) than those in maternal blood. All placental tissue obtained from first-trimester terminations of pregnancy assayed positive for IGF type 1 receptors. There was a direct correlation between neonatal weight and the levels of IGF-I (P < .02), but not with the levels of IGF-II. There were no significant correlations between newborn weights and IGFBP-3, or maternal serum levels of IGF-I and IGF-II. Amniotic fluid IGF-I and IGF-II levels were almost similar to fetal serum levels. CONCLUSION: These data demonstrate the presence of type 1 receptors and the bioavailability of IGF-I, IGF-II, and IGFBP-3 throughout pregnancy. Insulin-like growth factor-I is shown to be adjunctively and directly associated with fetal size in normal pregnancies. The precise role that IGFs play in deviant fetal growth or whether IGFs can be used to treat reduced fetal growth remains unknown and awaits further investigation.

Amniotic Fluid↗
PubMed2003

Circulating sodium pump inhibitors in five volume-expanded humans.

BACKGROUND: We have previously reported the isolation from human placentas of an inhibitor of the sodium pump (Na/K ATP-ase) of molecular weight 370 Da, which is considered to have a dihydropyrone-substituted steroid (bufenolide) structure. OBJECTIVE: To examine if this inhibitor is present outside of the pregnant state. METHODS: We examined the plasma ultrafiltrate of patients who were clinically volume-expanded. During the period of this study five such patients were identified. One was receiving haemofiltration for acute renal failure and four were being treated by plasma exchange. High performance liquid chromatograph (HPLC) purified fractions obtained from each of these five patients inhibited the human leucocyte sodium pump in vitro. RESULTS: Each of the purified fractions that inhibited the leucocyte ATP-ase in vitro contained a compound of mass 370 Da, the same mass as that found previously in placental extracts. This inhibitory factor was absent from HPLC purified fractions of plasma ultrafiltrate obtained from fifty-five patients who were clinically normovolaemic. Negative ion mass spectrometry (MS)/MS of the inhibitory material produced the fragmentation pattern characteristic of the placenta-derived pump inhibitor in only one of the five samples. The other four samples, although having the same mass, exhibited a different fragmentation pattern. CONCLUSION: The results suggest that an inhibitor of the sodium pump, identical in mass to that obtained from human placentas, circulates in the plasma of volume-expanded patients. The fragmentation pattern observed in negative ion mass spectrometry in the majority of the volume expanded patients may represent the presence of an isomer of the sodium pump inhibitor previously described in placental material.

Aged↗
PubMed1999

Expression of matrix metalloproteinases during murine chorioallantoic placenta maturation.

A large body of experimental evidence supports the participation of two groups of extracellular proteases, matrix metalloproteinases (MMPs), and plasminogen activators/plasmin, in tissue remodeling in physiological and pathological invasion. In the late mouse placenta, several tissue remodeling and cell invasion processes take place. Spongiotrophoblast migration into maternal decidua, as well as decidual extracellular matrix remodeling require the coordinated action of extracellular proteolytic enzymes. Via Northern and in situ hybridization, we have analyzed the spatio-temporal expression patterns of members of the MMP family (stromelysin-3, gelatinases A and B), as well as their inhibitors TIMP-1, -2 and -3 in late murine placenta (days 10.5 to 18.5 of gestation). Gelatinase activity in placental extracts was assessed by substrate zymography. Gelatinase A and stromelysin-3 were found to be prominently expressed in decidual tissue; shortly after midpregnancy, the decidual expression patterns of gelatinase A and stromelysin-3 became overlapping with each other, as well as with the expression domain of TIMP-2. On the other hand, gelatinase B transcripts were expressed only by trophoblast giant cells at day 10.5, and were downregulated at later stages. TIMP-1 and TIMP-3 transcripts were detected in decidual periphery at day 10.5, while later the expression was restricted to the endometrial stroma and spongiotrophoblasts, respectively. The areas of stromelysin-3 expression were the same (giant trophoblasts) or adjacent (decidua) to those where urokinase (uPA) transcripts were detected, suggesting a possible cooperation between these proteinases in placental remodeling. We generated mice doubly deficient for stromelysin-3 and uPA, and report here that these mice are viable and fertile. Furthermore, these animals do not manifest obvious placental abnormalities, thereby suggesting the existence of compensatory/redundant mechanisms involving other proteolytic enzymes. Our findings document the participation of MMPs and their inhibitors in the process of late murine placenta maturation, and warrant the characterization of other members of the MMP family, like membrane type-MMPs, in this process.

Allantoin↗
PubMed1991

Inhibin subunits in human placenta: localization and messenger ribonucleic acid levels during pregnancy.

This study describes the difference in distribution and levels of inhibin alpha, beta A- and beta B-subunit messenger ribonucleic acids in human placenta during pregnancy. Northern blot analysis indicated that inhibin alpha messenger ribonucleic acid is present in placental extracts collected at the early stage of gestation. Hybridization to inhibin beta A messenger ribonucleic acid was detected in the first trimester but in much lower levels. However, the intensity of the hybridization signal for inhibin alpha- and beta A-subunit messenger ribonucleic acids was greater in extracts prepared from term placentas than in those from the first or second trimester of pregnancy. Low levels of inhibin beta B-subunit messenger ribonucleic acid were observed only in extracts prepared from term placenta. At both early stage and term gestation trophoblast cells showed a positive fluorescent signal with the inhibin alpha-, beta A- and beta B-subunit-specific antisera. However, whereas inhibin alpha-subunit was localized in the cytotrophoblast, inhibin beta B-subunit immunoreactivity was observed in the syncytial layer of the villi, and inhibin beta A-subunit was widely distributed. The different distribution of immunoreactive inhibin subunits was confirmed by in situ hybridization, showing the different localizations of the inhibin messenger ribonucleic acids. These results showed that (1) human placenta produces the inhibin alpha- and beta A-subunits as early as the first trimester of pregnancy, (2) messenger ribonucleic acid levels for each of the three inhibin subunits are highest at term, and (3) immunoreactive inhibin subunits are localized differently in placental villi.

Female↗
PubMed1993

Biological and immunological activities of bovine placental gonadotropin.

A bovine placental extract was fractionated on a Concanavalin A (ConA)-Sepharose column into an unadsorbed ConA I fraction and an adsorbed ConA II fraction. The ConA II fraction was then separated by gel filtration on Sephadex G-100 into void volume material (ConA II Sephadex fraction I) and retarded material (ConA II Sephadex fraction II). Con A II Sephadex fraction II was considerably more potent than ConA II Sephadex fraction I in stimulating testosterone production by isolated rat Leydig cells. Con A I fraction was inactive in this regard. None of the aforementioned fractions manifested follicle stimulating hormone (FSH) bioactivity. ConA II Sephadex fraction II yielded a displacement curve parallel to the standard curve in radioimmunoassays for rat luteinizing hormone and thyroid stimulating hormone (TSH), but it did not cross-react in a radioimmunoassay for rat FSH. ConA II fraction did not exhibit FSH bioactivity. The results indicate that bovine placental gonadotropin possesses luteinizing hormone-like bioactivity and immunoreactivity and TSH immunoreactivity but neither FSH bioactivity nor immunoreactivity.

Animals↗