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PubMed1978

Control of placental 3 beta-hydroxy-delta 5-steroid dehydrogenase: partial characterization of an endogenous inhibitor and an endogenous activator.

Two substances which affect the activity and kinetic characteristics of 3 beta-hydroxy-delta 5-steroid dehydrogenase (delta 5-3 beta-HSD) have been recovered from homogenates of term human placenta by extraction with organic solvents after ethanol precipitation of protein. One of these substances, an inhibitor of the enzyme, is a non-polar unstable substance, which dialyzes through a cellulose nitrate membrane and which appears to be present in the tissue both in the free state and bound to either the enzyme or the microsomal membrane. It was not possible to produce a delta 5-3 beta-HSD preparation free of the inhibitor. The other substance is an activator, polar and stable with a molecular weight of less then 500, which increases both the apparent Km and the apparent V max of delta 5-3 beta-HSD. It is postulated that both substances play a part in control of placental progesterone synthesis.

3-Hydroxysteroid Dehydrogenases↗
PubMed2005

Placental cord drainage after spontaneous vaginal delivery as part of the management of the third stage of labour.

BACKGROUND: Cord drainage in the third stage of labour involves unclamping the previously clamped and separated umbilical cord and allowing the blood from the placenta to drain freely into an appropriate receptacle. Currently there are no systematic reviews of the effects of placental cord drainage on the management of the third stage of labour. OBJECTIVES: The objective of this review was to assess the specific effects of placental cord drainage on the third stage of labour, with or without the prophylactic use of oxytocics. SEARCH STRATEGY: We searched the Cochrane Pregnancy and Childbirth Group Trials register (July 2005), CINAHL (1982 to December 2004) and the National Research Register (December 2004). SELECTION CRITERIA: Randomised trials involving placental cord drainage as a variable within the package of interventions as part of the management of the third stage of labour. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed the quality of trials and extracted data. MAIN RESULTS: Two studies met our inclusion criteria in terms of quality and relevance. Cord drainage could impact the third stage of labour as the results show a statistically significant reduction in the length of third stage of labour (one trial, n = 147, weighted mean difference (minutes) -5.46, 95% confidence interval (CI) -8.02 to -2.90). In the incidence of retained placenta at 30 minutes after birth (one trial, n = 477, relative risk 0.28, 95% CI 0.10 to 0.73) a significant difference was found, but this should be interpreted with caution due to potential intervention bias. AUTHORS' CONCLUSIONS: It is difficult to draw conclusions from such a small number of studies, especially where the review outcomes were presented in a variety of formats. However, there does appear to be some potential benefit from the use of placental cord drainage in terms of reducing the length of the third stage of labour. More research is required to investigate the impact of cord drainage on the management of the third stage of labour.

Constriction↗
PubMed1986

Thyroid hormone receptors bind to defined regions of the growth hormone and placental lactogen genes.

The intracellular receptor for thyroid hormone is a protein found in chromatin. Since thyroid hormone stimulates transcription of the growth hormone gene through an unknown mechanism, the hypothesis that the thyroid hormone-receptor complex interacts with defined regions of this gene has been investigated in a cell-free system. Nuclear extracts from human lymphoblastoid IM-9 cells containing thyroid hormone receptors were incubated with L-3,5,3'-tri[125I]iodothyronine and calf thymus DNA-cellulose. Restriction fragments of the human growth hormone gene were added to determine their ability to inhibit labeled receptor binding to DNA-cellulose. These fragments encompassed nucleotide sequences from about three kilobase pairs upstream to about four kilobase pairs downstream from the transcription initiation site. The thyroid hormone-receptor complex bound preferentially to the 5'-flanking sequences of the growth hormone gene in a region between nucleotide coordinates -290 and -129. The receptor also bound to an analogous promoter region in the human placental lactogen gene, which has 92% nucleotide sequence homology with the growth hormone gene. These binding regions appear to be distinct from those that are recognized by the receptor for glucocorticoids, which stimulate growth hormone gene expression synergistically with thyroid hormone. The presence of thyroid hormone was required for binding of its receptor to the growth hormone gene promoter, suggesting that thyroid hormone renders the receptor capable of recognizing specific gene regions.

Base Sequence↗
PubMed1977

[Isolation and characterization of the placental protein pp5 (author's transl)].

The isolation and characterization of placemental protein PP5 is described. The purification was achieved by use of immunoadsorbents. From the tissue of one human term placenta an average amount of 15 mg PP5 can be extracted. PP5 apparently is specific for the placenta; it could not be detected in extracts from other human tissues. In sera from pregnant women PP5 is not present or only in trace amounts (less than 0.1 mg%). In the ultracentrifuge PP5 was found to have a sedimentation coefficient of 2.8 S and a molecular weight of 36,600 daltons. Electrophoretically the protein migrates as a fast beta1-globulin. The isoelectric point was determined to be 4.6. PP5 is a glycoprotein and contains 19.8% carbohydrates (hexoses 10.0%, hexosamine 4.4%, fucose 0.4%, sialic acid 5.0%). The amino acid composition of the protein is reported, too. PP5 was found to inhibit the activity of trypsin and plasmin; the biological role of this protein therefore may be the inhibition of proteases.

Female↗
PubMed2003

Puralpha, a single-stranded deoxyribonucleic acid binding protein, augments placental lactogen gene transcription.

Placental lactogen (PL) is thought to alter maternal metabolism to increase the pool of nutrients available for the fetus and to stimulate fetal nutrient uptake. The ovine (o) PL gene is expressed in chorionic binucleate cells (oBNC) and cis-elements located within the proximal promoter (-124 to +16 bp) are capable of trophoblast-specific expression in human (BeWo) and rat (Rcho-1) choriocarcinoma cells. Protein-DNA interactions were identified with oBNC nuclear extracts, and mutational analysis of these regions revealed a previously undefined cis-element from -102/-123 bp that enhances promoter activity in BeWo cells but not Rcho-1 cells. Characterization of this region identified the nucleotide sequence CCAGCA (-105/-110; o110) as the responsible cis-acting element. Southwestern analysis with this element identified a binding protein with an apparent M(r) of approximately 41,000. Expression screening of an ovine placental cDNA library identified six homologous cDNAs, which shared identity with human (97%) and mouse (95%) Pur alpha, a single-stranded DNA binding protein. The Pur alpha-o110 interaction was confirmed by electrophoretic mobility-supershift assays with oBNC and BeWo extracts but was absent with Rcho-1 extracts. Furthermore, overexpression of ovine Pur alpha enhanced transactivation of the oPL gene proximal promoter in both choriocarcinoma cell lines through this novel cis-element. This study identified a previously undefined cis-element, which interacts with Pur alpha to augment PL gene transcription.

3' Untranslated Regions↗
PubMed1994

Aromatization of 7 alpha-methyl-19-nortestosterone by human placental microsomes in vitro.

Part of the biological effects of testosterone (T) are mediated by its enzymatic reduction to 5 alpha-dihydrotestosterone (DHT) or aromatization to estradiol (E2). 7 alpha-Methyl-19-nortestosterone (MENT) is a synthetic androgen that is considerably more potent than T. Previous studies have shown that MENT is not 5 alpha-reduced. The studies reported here were undertaken to determine whether MENT undergoes enzymatic aromatization in vitro. Human placental microsomes were used as the source of the aromatase. Radioactive or nonradioactive T or MENT was incubated with the microsomes in the presence of NADPH and the metabolites extracted out with ethyl ether. Following evaporation of ether, the residue was dissolved in benzene-petroleum ether and extracted with 0.4 N NaOH which selectively removes phenolic metabolites of the androgens. When either radioactive T or MENT was incubated with the aromatase in the presence of NADPH, there was a 20-fold increase in the amount of radioactivity extracted with NaOH. In contrast, if the incubation was carried out in the absence of NADPH or in the presence of R76713, an aromatase inhibitor, most of the radioactivity remained in the benzene-petroleum ether phase. To further identify the enzymatic reaction products, thin layer chromatography (TLC) was performed. The Rf value for MENT was 0.22 while that of the major reaction product was 0.34, which corresponded with the RF value of the estrogen, 7 alpha-methyl-estradiol (MeE2). This was further verified by using a second solvent system for the chromatographic separation. In an effort to ascertain whether the metabolites bind to estrogen receptors (ER), rat uterine cytosol was used. NaOH extracts of medium following incubation of nonradioactive MENT with microsomes showed competitive inhibition of [3H]E2 binding to rat uterine ER. Furthermore, after [3H]MENT was incubated with microsomes, the radioactive metabolite extracted in NaOH showed specific binding to the ER which could readily be displaced with E2 or MeE2. These results indicate that like T, MENT undergoes enzymatic aromatization.

Aromatase↗
PubMed1995

Determination of the prorelaxin nucleotide sequence and expression of prorelaxin messenger ribonucleic acid in the golden hamster.

The objectives of this study were to determine the nucleotide and derived amino acid sequences of hamster prorelaxin and to evaluate prorelaxin mRNA expression during gestation. Total RNA was extracted from tissues through use of guanidinium hydrochloride methodology. A 23-bp oligonucleotide pool derived from the N-terminal amino acid sequence of hamster prorelaxin and Day-14 placental RNA were used in 3' RACE methodology to generate a prorelaxin-specific cDNA. This cDNA fragment (940 bp) was utilized to screen a Day-16 hamster placental cDNA library, and a clone containing the entire coding region was identified. Nucleotide sequence analysis revealed a 531-bp open reading frame for preprorelaxin. The derived amino acid sequence contained a 22 amino acid signal peptide followed by a 155 amino acid prorelaxin sequence with a calculated molecular weight of 17,500. The derived prorelaxin amino acid sequence had 51.8%, 42.9%, 41.7%, and 38.2% homology with rat, human-1, human-2, and pig prorelaxins, respectively. Expression of prorelaxin mRNA during the latter half of gestation was evaluated by Northern and/or slot-blot analysis using the 940-bp cDNA fragment as a hybridization probe. Prorelaxin mRNA was first detected in the placenta on Day 8. Levels of the 900-bp transcript increased to a plateau on Days 10, 12, and 14 and subsequently increased further on Day 15. Prorelaxin mRNA was not detected in ovary, hippocampus, or neocortex.

Amino Acid Sequence↗
PubMed1998

Oncomodulin is expressed exclusively by outer hair cells in the organ of Corti.

Oncomodulin (OM) is a small, acidic calcium-binding protein first discovered in a rat hepatoma and later found in placental cytotrophoblasts, the pre-implantation embryo, and in a wide variety of neoplastic tissues. OM was considered to be exclusively an oncofetal protein until its recent detection in extracts of the adult guinea pig's organ of Corti. Here we report that light and electron microscopic immunostaining of gerbil, rat, and mouse inner ears with a monoclonal antibody against recombinant rat OM localizes the protein exclusively in cochlear outer hair cells (OHCs). At the ultrastructural level, high gold labeling density was seen overlying the nucleus, cytoplasm, and the cuticular plate of gerbil OHCs. Few, if any, gold particles were present over intracellular organelles and the stereocilia. Staining of a wide range of similarly processed gerbil organs failed to detect immunoreactive OM in any other adult tissues. The mammalian genome encodes one alpha- and one beta-isoform of parvalbumin (PV). The widely distributed alpha PV exhibits a very high affinity for Ca2+ and is believed to serve as a Ca2+ buffer. By contrast, OM, the mammalian beta PV, displays a highly attenuated affinity for Ca2+, consistent with a Ca2+-dependent regulatory function. The exclusive association of OM with cochlear OHCs in mature tissues is likely to have functional relevance. Teleological considerations favor its involvement in regulating some aspect of OHC electromotility. Although the fast electromotile response of OHCs does not require Ca2+, its gain and magnitude are modulated by efferent innervation. Therefore, OM may be involved in mediation of intracellular responses to cholinergic stimulation, which are known to be Ca2+ regulated. (J Histochem Cytochem 46:29-39, 1998)

Animals↗
PubMed2004

Selenium deficiency as a model of experimental pre-eclampsia in rats.

Epidemiological studies and in vitro analysis demonstrate correlations between selenium status and human pre-eclampsia (PET). Selenium is an essential component in the anti-oxidant proteins glutathione peroxidase and thioredoxin reductase, which are produced in lower amounts in pre-eclamptic placenta. This study examined the effect of modulating dietary selenium content in pregnant rats. Rats were fed diets containing no selenium, 239 microg/kg selenium or 1000 microg/kg selenium, four weeks prior to and following conception. Significant pregnancy-specific increases in systolic blood pressure (116.4 +/- 5.2 mmHg vs 108 +/- 6.8 mmHg vs 111.4 +/- 4.7 mmHg) and proteinuria (9.68 +/- 2.12 microg/ml vs 5.93 +/- 1.59 microg/ml vs 4.43 +/- 0.96 microg/ml) were demonstrated in animals fed a selenium free-diet when compared with normal or high selenium diets. Placental weight and pup number were not affected by selenium deprivation, however a significant decrease in the pup weight was evident. Selenium deprivation caused dose-dependent decreases in liver glutathione peroxidase (28.55 +/- 3.82 mmoles/min/mg vs 34.68 +/- 8.64 mmoles/min/mg) and thioredoxin reductase (2.37 +/- 1.25 U/mg vs 6.68 +/- 1.82 U/mg) activity, whereas superoxide dismutase activity remained constant. Placental activity of these enzymes also decreased leading to oxidative stress as measured by increased lipid peroxides (17.92 +/- 1.78 micromoles/mg vs 8.30 +/- 5.52 micromoles/mg) and protein carbonyls in tissue extracts from selenium-free animals. These results suggest that selenium deficiency in pregnant rats leads to symptoms similar to those seen in human PET and may provide an experimental model for studying this complex disease.

Animals↗
PubMedDate not supplied

[Study of the dynamic distribution of azafen in the organs and tissues by using direct fluorimetry].

A quantitative method of direct fluometry of the samples without any preliminary extraction of the preparation, devised by the authors helped demonstrate that after its intravenous administration the cyclic antidepressant azaphen rapidly penetrates via the blood-cerebral, blood-ophthalmic, placental and other blood-histological barrier and is then quickly eliminated from the organism.

Animals↗
PubMed2000

Localization of messenger ribonucleic acid for adrenomedullin and adrenomedullin receptor in the human placenta in normal pregnancies and pregnancies complicated by oligohydramnios.

OBJECTIVE: The purpose of this study was to identify the placental expression of adrenomedullin and adrenomedullin receptor messenger ribonucleic acid and compare them between placentas from pregnancies associated with oligohydramnios as a result of uteroplacental insufficiency and placentas from normal pregnancies. STUDY DESIGN: Total ribonucleic acid was extracted from the amnion, chorion, cotyledon, umbilical vein, and umbilical artery in 5 normal placentas and 3 placentas from pregnancies complicated by oligohydramnios. A cell line known to express messenger ribonucleic acid of adrenomedullin and its receptor was used to optimize the polymerase chain reaction and served as a positive control preparation in all experiments. Semiquantitative reverse transcriptase-polymerase chain reaction results for adrenomedullin and adrenomedullin receptor were compared between tissues as densitometric ratios of adrenomedullin or adrenomedullin receptor messenger ribonucleic acid to beta(2)-microglobulin messenger ribonucleic acid. Results were analyzed with a Kruskal-Wallis 1-way analysis of variance. Immunohistochemical staining with an antibody to human adrenomedullin was used to localize adrenomedullin in all tissue types. RESULTS: Messenger ribonucleic acid sequences for adrenomedullin and adrenomedullin receptor genes were identified in all tested placental tissue components. Within the normal placentas the expressions of adrenomedullin and adrenomedullin receptor messenger ribonucleic acid sequences did not differ statistically between the tissue components. Within placentas from patients with oligohydramnios the expressions of adrenomedullin and adrenomedullin receptor messenger ribonucleic acid did not differ statistically between the tissue components. When normal placentas were compared with placentas from pregnancies complicated by oligohydramnios, however, a 5-fold increase in adrenomedullin messenger ribonucleic acid and a 3-fold increase in adrenomedullin receptor messenger ribonucleic acid were seen in placentas from patients with oligohydramnios. Adrenomedullin immunoreactivity was present in all tissues studied. CONCLUSION: The expression of messenger ribonucleic acid for both adrenomedullin and its receptor in these tissue components implies that placental tissues function in both synthesis and action of adrenomedullin. The increased adrenomedullin messenger ribonucleic acid expression in the umbilical artery and the elevated adrenomedullin receptor messenger ribonucleic acid expression in the cotyledons of placentas from patients with oligohydramnios may represent a local fetoplacental physiologic adaptive response to vascular compromise.

Adrenomedullin↗
PubMed1978

Glucocorticoids and the rhesus fetal lung.

The effects of glucocorticoids on primate fetal lung function have not been clearly delineated. In this prospective study of preterm rhesus fetuses exposed in utero to betamethasone for 72 hours, the most significant alteration was a striking increase in maximum lung volumes. Functionally less significant increases in residual lung volumes were also noted. The lungs of the treated fetuses did not exhibit lower extract surface tensions or increased phospholipid concentrations. These findings suggest that the major effect of betamethasone is on lung connective tissue elements, with minimal effects on alveolar surfactant. Additional evidence of the multisystemic effects of glucocorticoids was obtained in that significant differences in fetal, adrenal, hepatic, and placental weights also were observed.

Amniotic Fluid↗
PubMed1995

Activin inhibits but inhibin activates mouse placental lactogen-II secretion.

The regulation of mouse placental lactogen (mPL)-I and mPL-II secretion by activin and inhibin and the expression of activin and inhibin subunit mRNAs in the mouse decidua were examined. Activin-A at a concentration of 10 nM/l significantly inhibited mPL-II secretion by placental cells from days 9 and 12 of pregnancy. However, activin-A did not affect mPL-I secretion by cells from days 7 and 9 of pregnancy nor mPL-II secretion by cells from day 7 of pregnancy. By contrast, 10 nM/l inhibin activated mPL-II secretion by cells from day 12 of pregnancy. These effects of activin and inhibin on mPL-II secretion were dose-dependent. Follistatin, which binds to activin and blocks its bioactivity, completely eliminated the inhibitory effect of activin on mPL-II secretion. Incubation of placental cells from day 12 of pregnancy with activin-A resulted in a significant reduction of the mPL-II mRNA level assessed by Northern blot analysis. Northern blot analysis using poly(A)+RNA extracted from the decidua indicated that mouse decidua, as well as the placenta, express all activin and inhibin subunits and that their gene expressions increased during gestation. The expression of these mRNAs in the decidua was much higher than those in the placenta. These findings suggest that activin and inhibin regulate mPL-II secretion and suggest the presence of an autocrine or paracrine regulation of mPL-II secretion in mouse placenta by activin and inhibin after mid-pregnancy in vivo.

Activins↗
PubMed1987

Characterization of lipocortin I and an immunologically unrelated 33-kDa protein as epidermal growth factor receptor/kinase substrates and phospholipase A2 inhibitors.

Reversible calcium-dependent association with a particulate fraction from human placenta was used as the first step in the purification of substrates for the epidermal growth factor-stimulated protein kinase. A protein with apparent Mr of 35,000 was purified to homogeneity, and the sequence was determined for approximately one-fourth of the protein. These residues could be aligned exactly with the previously published sequence of lipocortin I derived from the cDNA from a human lymphoma. Two other proteins that appear to be formed by proteolytic removal of 12 or 26 of the amino acids from the NH2 terminus of the protein also were isolated. Placental lipocortin I was phosphorylated in Tyr-21 in an epidermal growth factor-dependent manner by the kinase activity in a particulate fraction from A431 cells; half-maximal phosphorylation occurred at 50 nM lipocortin I. Lipocortin I phosphorylated on Tyr-21 was approximately 10-fold more sensitive to tryptic cleavage at Lys-26 than was the native protein. Placental lipocortin I and its two truncated forms were potent inhibitors of pancreatic phospholipase A2 activity. Another 33-kDa protein that was not related immunologically to lipocortin I or lipocortin II (calpactin I) also was purified from the EGTA extract of placenta. The unidentified protein inhibited phospholipase A2 but was not a substrate for the epidermal growth factor-stimulated kinase. The mechanism by which these proteins inhibit phospholipase A2 activity was investigated. Attempts to detect direct interaction between these proteins and the enzyme were unsuccessful. However, both the unidentified protein, lipocortin I, and 32P-labeled lipocortin I bound in a Ca2+-dependent manner to the [3H]oleic acid-labeled Escherichia coli membranes used as substrate in the phospholipase A2 assay. Heparin, which is known to block lipocortin I inhibition of phospholipase A2, also blocked binding of lipocortin I to E. coli membranes. The results of these and other experiments raise the possibility that placental lipocortin I inhibits phospholipase A2 activity in this assay by coating the phospholipid and thereby blocking interaction of enzyme and substrate.

Amino Acid Sequence↗
PubMed2005

Amniotic IGF-I supplementation of growth-restricted fetal sheep alters IGF-I and IGF receptor type 1 mRNA and protein levels in placental and fetal tissues.

We have previously reported that chronic intra-amniotic supplementation of the late gestation growth-restricted (IUGR) ovine fetus with IGF-I (20 microg/day) increased gut growth but reduced liver weight and circulating IGF-I concentrations. Here we report mRNA and protein levels of IGF-I, the type 1 IGF receptor (IGF-1R) and IGF-binding proteins (IGFBP)-1, -2 and -3 in fetal gut, liver, muscle and placenta from fetuses in that earlier study in an attempt to explain these contrasting results. mRNA and protein were extracted from tissues obtained at post mortem at 131 days of gestation (term, 145 days) from three groups of fetuses (control, IUGR+saline and IUGR+IGF-I, n=9 per group). Control fetuses were unembolised and untreated. In the IUGR groups, growth restriction was induced from 113 to 120 days by placental embolisation; from 120 to 130 days fetuses were treated with daily intra-amniotic injections of either saline or 20 microg IGF-I. mRNA was measured by RT-PCR or real-time RT-PCR, and protein by Western blot. In liver, muscle and placenta, IGF-I mRNA and protein levels were reduced by between 8 and 30% in IGF-I-treated fetuses compared with saline-treated fetuses and controls with no change in IGF-1R mRNA or protein levels. In contrast, in the gut, IGF-I mRNA and protein levels were not significantly altered with IGF-I treatment, but IGF-1R levels were increased, especially in the jejunum. Immunolocalisation demonstrated that IGF-1R expression was confined to the luminal aspect of the gut. mRNA levels of all three IGFBPs were reduced in the gut of IGF-I-treated fetuses, but hepatic expression was significantly increased. These data demonstrated tissue-specific regulation of IGF-I, IGF-1R and IGFBPs-1, -2 and -3 in response to intra-amniotic IGF-I supplementation, though the underlying mechanisms remain obscure.

Amniotic Fluid↗
PubMed1996

Expression of atrial natriuretic peptide by third-trimester placental cytotrophoblasts in women.

Atrial natriuretic peptide (ANP) is a vasoactive molecule with a potential role in modulating uteroplacental blood flow. We examined the expression of ANP in the third-trimester fetomaternal interface by immunohistochemistry performed on sections of placental tissue as well as by reverse transcriptase-polymerase chain reaction (RT-PCR) and RIA performed on isolated, purified term trophoblasts. Results from immunohistochemical studies on ten normal term placental samples revealed labeling of extravillous interstitial and cytotrophoblastic shell trophoblasts. The trophoblastic identity of the cells was determined by labeling of adjacent serial sections with anti-cytokeratin antibody. Labeling of decidual tissue was also observed in some samples (3 of 10 samples), whereas villous trophoblastic tissue showed no labeling. RT-PCR analysis of RNA extracted from isolated third-trimester trophoblasts revealed the presence of a 0.45-kb and band corresponding to ANP mRNA. Sequencing of the amplified cDNA confirmed its identity. RIA on lysates of isolated trophoblasts revealed the presence of ANP at a level of 41 pg +/- 8 pg/10(7) cells (n = 4; range = 16.8-50.4 pg/10(7) cells). These results indicate that placental cytotrophoblastic tissue is a source of ANP. This molecule might play a role in the regulation of uteroplacental and/or fetoplacental blood flow.

Atrial Natriuretic Factor↗
PubMed2005

Altered expression of IGFs and IGF-binding proteins during intrauterine growth restriction in guinea pigs.

The IGF system is one of the most important endocrine and paracrine growth factor systems that regulate fetal and placental growth. We hypothesized that intrauterine growth restriction (IUGR) in guinea pigs is mediated by the altered expression of IGFs and/or IGF binding protein (BP) mRNAs in tissues and is related to growth of specific tissues. IUGR was induced by unilateral uterine artery ligation on day 30 of gestation, and fetal plasma, amniotic fluid and tissue samples were collected at 55-57 days (term about 68 days) from paired IUGR and control fetuses (n=6). Western ligand blotting and immunoblotting were used to compare IGFBP levels in plasma and amniotic fluid. Total RNA was extracted from placenta and fetal tissues, and the relative abundance of IGF-II and IGFBP-1-6 mRNA was determined by Northern blotting, using species-specific probes where available. IUGR fetuses had decreased (P<0.01, by Student's t-test) placental weight and body weight with an increase in the brain:liver weight ratio. The principal IGFBPs in fetal plasma migrated at 40-35, 30 and 25 kDa and were identified as IGFBP-3, -2 and -4 respectively. IUGR was associated with elevated plasma IGFBP-2 and IGFBP-4 and reduced IGFBP-3 levels. IGFBPs were detected at low levels in amniotic fluid of control fetuses but at higher levels in IUGR fetuses. In IUGR placentae, there was a small increase in IGFBP-4 mRNA (P<0.05). IGFBP-2 mRNA increased (P<0.001) in liver of IUGR fetuses. IGF-II and IGFBP mRNA expression did not change in fetal muscle. The results are consistent with reduced IGF action, directly or through inhibition by IGFBPs, particularly by circulating and tissue IGFBP-2, as a potential causal factor in decreased growth of the placenta and certain fetal tissues.

Amnion↗