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At least 451 records · Page 25Linked to original sources
PubMed1987

Epidermal growth factor (EGF)-like transforming growth factor (TGF) activity and EGF receptors in ovine fetal tissues: possible role for TGF in ovine fetal development.

To determine whether epidermal growth factor (EGF) or EGF-like transforming growth factors (TGFs) are present in ovine fetal tissues, we have tested acid-ethanol extracts of ovine fetal kidney for the ability to induce anchorage-independent growth of normal rat kidney fibroblasts in soft agar and to compete with 125I-mouse EGF for binding to receptors in sheep liver. The fetal kidney extract (20-1000 micrograms protein/ml) stimulated a dose-dependent increase in the number of soft agar colonies of normal rat kidney cells. Approximately 70% of these colonies measured greater than or equal to 3100 microM2. The fetal kidney extract was dissolved in 1 M acetic acid and chromatographed on Bio-Gel P 10. Two peaks of TGF-like activity, with approximate MW 14.5K (peak 1) and 9K (peak 2), eluted from the column. Half-maximal effects of pooled peaks 1 and 2 on colony formation were achieved using 100 and 20 micrograms protein/ml, respectively. Peaks 1 and 2 also competed with 125I-mouse EGF for binding to EGF receptors in ovine fetal liver but had no activity in a homologous mouse EGF radioimmunoassay sensitive to 15 pg mouse EGF. Neither TGF activity nor EGF receptor binding activity was detected in Bio-Gel fractions co-eluting with 125I-mouse EGF. Specific 125I-EGF binding sites in fetal liver were detected as early as midgestation, and the number of EGF binding sites increased markedly in late gestation, exceeding the number of EGF binding sites in the livers of pregnant ewes. These findings demonstrate the presence of TGF-like activity in ovine fetal kidney and high affinity EGF receptors in ovine fetal liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Gestational changes of thyroid hormone action in the developing fetal bovine epiphysis.

Thyroid hormones are essential for cartilage growth and maturation. In order to assess their actions during different periods of skeletal development, [125I]-triiodothyronine (T3) binding capacity in epiphyseal cartilage and triiodothyronine concentrations in serum were quantitated in bovine fetuses of the second and third trimesters of gestation (equivalent to fetal sizes of 10-90 cm crown-rump (CR) length), and related to the alkaline phosphatase activities in the same cartilaginous tissues. Nuclear T3 binding levels, which were initially low during 10-30 cm CR, rose to a peak value (1.7 pmol/mg DNA) at the end of the second trimester (40-50 cm CR). Then, following a sharp decline at 50-60 cm CR, T3 binding rose to a moderate level in the later gestational period (60-90 cm CR). Serum total triiodothyronine rose transiently in fetuses of 30-50 cm CR to a peak level (34 ng/100 ml), and subsequently increased continuously in the later period (60-90 cm CR). Alkaline phosphatase activities measured in epiphyseal chondrocytes rose significantly in fetuses of 60-90 cm CR. The coincident rise of cartilage triiodothyronine binding capacity and serum circulating triiodothyronine levels in the late second trimester suggests that this thyroid hormone induces its own binding sites in bovine epiphyseal cartilage; the dramatic increase in the level of serum triiodothyronine during the third trimester of gestation is temporally related to the increase in alkaline phosphatase activity of chondrocytes, as well as other recognized developmental changes in the fetal bovine skeletal tissues.

Alkaline Phosphatase↗
PubMed1998

Assessing the effects of low boron diets on embryonic and fetal development in rodents using in vitro and in vivo model systems.

To date, boron (B) essentiality has not been conclusively shown in mammals. This article summarizes the results of a series of in vitro and in vivo experiments designed to investigate the role of B in mammalian reproduction. In the first study, rat dams were fed either a low (0.04 microg B/g) or an adequate (2.00 microg B/g) B diet for 6 wk before breeding and through pregnancy; reproductive outcome was monitored on gestation day 20. Although low dietary B significantly lowered maternal blood, liver, and bone B concentrations, it had no marked effects on fetal growth or development. The goal of the second study was to assess the effects of B on the in vitro development of rat postimplantation embryos. Day 10 embryos collected from dams fed either the low or adequate B diets for at least 12 wk were cultured in serum collected from male rats exposed to one of the two dietary B treatments. Dams fed the low B diet had a significantly reduced number of implantation sites compared to dams fed the B-adequate diet. However, embryonic growth in vitro was not affected by B treatment. The aim of study 3 was to define the limits of boric acid (BA) toxicity on mouse preimplantation development in vitro. Two-cell mouse embryos were cultured in media containing graded levels of BA (from 6 to 10,000 microM). Impaired embryonic differentiation and proliferation were observed only when embryos were exposed to high levels of BA (>2000 microM), reflecting a very low level of toxicity of BA on early mouse embryonic development. Study 4 tested the effects of low (0.04 microg B/g) and adequate (2.00 microg B/g) dietary B on the in vitro development of mouse preimplantation embryos. Two-cell embryos obtained from the dams were cultured in vitro for 72 h. Maternal exposure to the low B diet for 10, 12, and 16 wk was associated with a reduction in blastocyst formation, a reduction in blastocyst cell number, and an increased number of degenerates. Collectively, these studies support the concept that B deficiency impairs early embryonic development in rodents.

Animals↗
PubMed1995

SPARC participates in the branching morphogenesis of developing fetal rat lung.

Adhesion of cells to components of the extracellular matrix has been shown to be critical in normal lung development, particularly during the pseudoglandular stage, when conducting airways are forming through a process of branching morphogenesis. Expression of factors that inhibit cellular adhesion might also modulate branching morphogenesis. SPARC is a secreted glycoprotein that exhibits antiadhesive effects on cultured cells and is widely expressed in embryonic tissues. In this report, we examine the distribution of SPARC in fetal rat lung during development and its effect on the process of branching morphogenesis. Immunohistochemistry and in situ hybridization studies revealed that SPARC was present in the airway epithelial cells during the pseudoglandular stage of lung development, and in blood vessels and smooth muscle cells associated with airways during the canalicular and saccular stages of development. We used an in vitro model of rat lung branching morphogenesis to examine airway branching in the presence of: a) a neutralizing anti-SPARC antibody; or b) a synthetic peptide from a region of SPARC that, like the native protein, perturbs cell adhesion and diminishes the synthesis of fibronectin and thrombospondin 1. Lungs cultured in the presence of either reagent exhibited diminished branching and an abnormal morphology that was characterized in part by dilated airways. These findings implicate SPARC in the development of the airways.

Amino Acid Sequence↗
PubMedDate not supplied

Influence of N-3-pyridoyltryptamine (tryptamide) on fetal development in rats and mice.

N-3-pyridoyltryptamine (Tryptamide, TRP) was examined for embryotoxic and teratogenic activities in rats and mice. Female Wistar rats and Albino Swiss mice were given TRP per os on days 6-14 of gestation. The rats were killed on day 21, and mice on day 18 of pregnancy. The general health and reproduction of females were evaluated, and fetuses were examined and processed to characterize external, visceral and skeletal malformations. TRP given to mothers in doses of 10 to 500 mg/kg po did not produce statistically significant embryotoxic or teratogenic effects in rats. It was not teratogenic also in mice but in this species the dose of 500 mg/kg produced embryotoxic effects.

Animals↗
PubMed1987

In utero morphological effects of hydroxyurea on the fetal development in Sprague-Dawley rats.

In order to investigate in utero morphological effect of hydroxyurea (HU) in Sprague-Dawley rats, HU was intraperitoneally injected to pregnant Sprague-Dawley rats at a dose of 100 or 200 mg/kg/day during the organogenetic period (days 9-12 of gestation). A dose of 200 mg/kg/day induced growth retardation, high mortality and high incidence of malformations, although a dose of 100 mg/kg/day produced no adverse effects in the next generation. In the HU 200 mg/kg/day group the incidence of malformations in pups at 4 days of age was low as compared with that in fetuses and pups at 21 days of age. Increasing perinatal mortality in fetuses and pups due to severe central nervous system (CNS) malformations and disappearance of some cases of ventricular septal defect after delivery were considered as the possible causes to induce difference in malformation rate in various stage of development. Latent effect on the development of CNS malformations was observed between 4 and 21 days of age. There was no sex difference in teratogenic effect. These findings were compared with those in Wistar rats exposed to HU 200 mg/kg/day. The incidence of perinatal malformations and the stillbirths were significantly higher in the Wistar rats as compared with those in the Sprague-Dawley rats. In addition, such morphological effects of HU as the exencephaly, dilatation of lateral ventricle, anophthalmia, cleft palate and micrognathia are less severe in Sprague-Dawley rat fetuses than in Wistar rat fetuses.

Abnormalities, Drug-Induced↗
PubMed1983

Plasmalemmal vesicles in pulmonary capillary endothelium of developing fetal lamb lungs.

In adult mammalian lungs pinocytotic vesicles (PV) play a role in macromolecular transport across endothelium. The time course of their development in fetal lungs was examined. Morphometric techniques were used to measure the relative capillary volume as percentage of lung volume. Mean diameter (D), numerical density (Nv), and endothelial fractional volume (Vv) represented by PV were determined in randomly selected capillaries, measuring 5.3-8.4 microns in diameter, from right upper (RUL) and left lower (LLL) lobes of lungs from fetal lambs ranging in gestational ages from 39 to 144 days. Three newborn lambs, 1 hr after birth, were also examined. There was a 20-fold increase in the volume density of capillaries during the period studied. The vesicular D +/- SD was 739.6 +/- 4.1 and 735.1 +/- 2.8 A in RUL and LLL, respectively, and remained unchanged throughout gestation. By contrast, following a gradual increase in Nv from 24.7 to 65.1/microns3 in the glandular stage (39-85 days), there was a rapid rise in Nv during both canalicular (95-121 days) and alveolar (130-144 days) stages of development, reaching a final Nv of 254.8/microns3. In newborn lambs, 1 hr after birth, there was no significant change in Nv. There was a significant correlation between Nv and fetal age, but there was no difference in Nv between RUL and LLL at any time. Thus, a more than 10-fold increase in Nv of PV occurs in ovine pulmonary capillary endothelium during gestation, the biochemical and/or physiological basis of which remains to be determined. By contrast, observations made on coated vesicles indicate that Nv of these structures does not change with gestation.

Animals↗
PubMed1988

[Variants of pathological immaturity of the placenta and their role in fetal development].

Morphologic evaluation of 125 placentas in various pregnancy and neonatal disturbances versus 46 normal placentas of different gestation provided the basis for recognition of 4 basic variants of the villous tree immaturity. Variant I is marked by embryonal villi close in structure to the villi of normal placentas (8-12 weeks gestation). Variant II presents intermediate immature and mature branches demonstrating the morphology of mean-caliber placental villi (13-28 weeks gestation). Variant III involves irregular sclerosed villi (23-24 weeks gestation). These variants are concerned with pathologic placental immaturity. There is also another variant which is confirmed by the evidence gained and can be related to a borderline condition between health and pathology--dissociated placentation. A favourable neonatal prognosis depends on a large amount of terminal special villi and compensatory placental angiomatosis.

Abortion, Spontaneous↗
PubMed1998

Sustained hyperglycemia in vitro down-regulates the GLUT1 glucose transport system of cultured human term placental trophoblast: a mechanism to protect fetal development?

The trophoblast of human placenta is directly exposed to the maternal circulation. It forms the main barrier to maternal-fetal glucose transport. The present study investigated the effect of sustained hyperglycemia in vitro on the glucose transport system of these cells. Trophoblasts isolated from term placentas and immunopurified were cultured for 24, 48, and 96 h in DMEM containing either 5.5 (normoglycemia) or 25 mmol/l D-glucose (hyperglycemia), respectively. Initial uptake of glucose was measured using 3-O-[14C]methyl-D-glucose. Kinetic parameters were calculated as K(M) = 73 mmol/l and Vmax = 29 fmol s(-1) per trophoblast cell. Uptake rates of cells cultured under hyperglycemic conditions did not differ at exogenous D-glucose concentrations in the physiological range (1, 5.5, 10, and 15 mmol/l), but were significantly decreased by 25% (P<0.05) at diabetes-like concentrations (20 and 25 mmol/l) as compared to normoglycemic conditions. This effect was due to a decrease in Vmax (-50%), whereas K(M) remained virtually unaffected. GLUT1 mRNA levels were lower by 50% (P<0.05; Northern blotting) and GLUT1 protein was reduced by 16% (P<0.05; Western blotting) in trophoblast cells cultured under hyperglycemic vs. normoglycemic conditions. We conclude that prolonged hyperglycemia in vitro reduces trophoblast glucose uptake at substrate concentrations corresponding to blood levels of poorly controlled diabetic gravidas. This effect is due to diminished GLUT1 mRNA and protein expression in the trophoblast.

3-O-Methylglucose↗
PubMedDate not supplied

Leptin levels in maternal and cord serum: relationship with fetal development and placental weight.

OBJECTIVE: To test the hypothesis that the circulating levels of leptin in the maternal and cord serum correlate with the birthweight of the newborns and with the weight of the placenta. METHODS: In a population of 85 women from northern Greece who gave birth to an equal number of full-term infants, we calculated the concentration of leptin in the maternal serum as well as in the cord serum, right after delivery, by using an immunoradiometric assay. The correlation between these values, the maternal BMI before pregnancy and at the time of delivery, the neonatal BMI, Ponderal Index, and the placental weight was studied. RESULTS: Mean maternal leptin showed a statistically significant difference from mean cord serum leptin (14.7 and 7.07 ng/ml, respectively) and was positively correlated to the maternal BMI at the time of delivery (r = 0.3, P = 0.016), but not to neonatal BMI. A positive correlation between the mean cord serum leptin and the BMI of the neonates (r = 0.26, P = 0.031 ) was found. There was no correlation between the maternal BMI at the time of delivery and the neonatal BMI. Similarly, no correlation could be established between the placental weight and the levels of leptin in the maternal or in the cord serum but a positive correlation between placental weight, neonatal BMI and weight, and mothers' BMI was observed. Finally, although a noteworthy difference between the mean leptin levels of neonates of two different sexes was observed (male 5.9 ng/ml, female 7.8 ng/ml), that difference never reached a statistically significant level. CONCLUSIONS: The maternal leptin level could not be used as a reliable marker of fetal growth but a positive correlation between cord serum leptin and fetus growth is suggested.

Adult↗
PubMed2000

Cisplatin-DNA adduct formation in rat spermatozoa and its effect on fetal development.

Exposure of males to some genotoxic chemicals causes DNA damage in spermatozoa resulting in embryotoxicity and developmental defects in their offspring. This study demonstrates that cisplatin-DNA adducts could be measured in spermatozoa following treatment with the antineoplastic drug, cisplatin. The formation of spermatozoa cisplatin-DNA adducts showed dose and time-dependent increases both in vitro, and in vivo up to 168 h (7 days) after dosing. Treatment of rats with 10 mg cisplatin/kg resulted in spermatozoa Pt-GG adduct levels of approximately 1.0 fmol/microg DNA. When cisplatin-treated male rats were bred to untreated females 6-24 h after cisplatin administration, no adverse developmental effects or decreases in body weight were seen in the offspring although there was a trend towards increased early embryo mortality.

Animals↗
PubMed1991

Programmed demethylation in CpG islands during human fetal development.

The mechanism for establishing the DNA methylation patterns observed in adult mammalian tissues is not well understood. To determine when adult patterns are established for housekeeping genes, we examined the clustered CpGs in genes on the human active X chromosome (PGK, G6PD, P3, GdX, HPRT) and the autosomal gene, DHFR. We find unique methylation patterns present at the P3 locus in all tissues analyzed from 6- to 9-week fetal specimens, and at the HPRT locus in adrenal gland DNA at this stage of development. Adult patterns are established subsequently by demethylating specific CpGs. Our results show that demethylating events affecting CpG islands are programmed during mammalian fetal development. They suggest that the process of de novo methylation in the fetus methylates at least some sites in the 3' region of the CpG islands in active genes and that adult patterns are established at 6-14 weeks developmental age by sequence-specific demethylation.

Blotting, Southern↗