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PubMed1981

Procollagen messenger RNA levels and activity and collagen synthesis during the fetal development of sheep lung, tendon, and skin.

The rates of type I collagen synthesis in sheep lung, tendon, and skin were evaluated during the latter half of fetal development and compared with the levels of type I procollagen mRNA, quantified by molecular hybridization with a type I procollagen specific complementary DNA, and with the activity of total procollagen mRNA measured by in vitro cell-free translation. In the lung and tendon, the levels of type I procollagen mRNA and activity of total procollagen mRNA parallel collagen synthesis during development. In the skin, however, type I collagen synthesis declines sharply during fetal development, but both type I procollagen mRNA levels and total procollagen mRNA activity remain at the high levels of early development. These observations suggest that in developing lung and tendon, type I procollagen mRNA levels are likely the major determinants of the levels of type I collagen synthesis. In contrast, the dichotomy between type I procollagen mRNA levels and rates of type I collagen synthesis in the developing sheep skin suggest the skin utilizes mechanisms in addition to mRNA levels to modulate expression of the type I collagen gene.

Animals↗

PubMed1986

Retinol-binding protein and transthyretin mRNA levels in visceral yolk sac and liver during fetal development in the rat.

Studies were conducted to explore the synthesis of retinol-binding protein and transthyretin by embryonic and extraembryonic tissues during fetal development in the rat. The levels of retinol-binding protein mRNA and transthyretin mRNA were measured in fetal liver and in extraembryonic tissues by RNA gel blot analysis and hybridization with specific cDNA probes. Retinol-binding protein mRNA and transthyretin mRNA were both detected in the liver of fetuses at 14 days of gestation. The relative levels of these two transcripts increased during later fetal development; by the 20th day of gestation retinol-binding protein mRNA levels were comparable to those of the adult liver, while the levels of transthyretin mRNA were only 46% of those of the adult liver. Examination of the extraembryonic membranes for retinol-binding protein mRNA and transthyretin mRNA showed that these two transcripts were present specifically and only in the visceral yolk sac. The relative levels of retinol-binding protein mRNA and transthyretin mRNA in visceral yolk sac were constant from 14 to 20 days of gestation, averaging 58% and 51%, respectively, of the adult liver levels of these two transcripts. Both retinol-binding protein mRNA and transthyretin mRNA in the visceral yolk sac were found to be specifically localized in the endodermal layer. Finally, both immunoprecipitable retinol-binding protein and transthyretin were found to be synthesized and secreted by explant cultures of visceral yolk sac tissue. These data show that the visceral yolk sac is a major source of both retinol-binding protein and transthyretin in the developing fetus. Since the visceral yolk sac is a site of true placentation and nutrient transfer in the rodent, this raises the possibility that visceral yolk sac-derived retinol-binding protein and transthyretin may play important roles in the transport and delivery of retinol from the maternal blood to the developing fetus.

Animals↗

PubMed1989

[The influence of circulatory failure on fetal development in women with rheumatism].

In the time-course of pregnancy the characteristic features of fetal development were studied in 149 females with rheumatic disease with the employment of ultrasonic fetometry. Certain features of growth in various anatomical structures of the fetus with regard to the stage of decompensation were identified Four-staged impairments in the development of the fetuses were revealed in this contingent.

Embryonic and Fetal Development↗

PubMed1995

Expression of parathyroid hormone-related peptide and its receptor messenger ribonucleic acids during fetal development of rats.

PTH-related peptide (PTHrP) is a causative agent of hypercalcemia associated with malignancy. PTHrP binds to and activates the same receptor as does PTH. Because PTHrP has been suggested to regulate the growth and differentiation of cells as a paracrine/autocrine factor, we examined the expression of both PTHrP and its receptor genes during fetal development of rats (15-20 days gestation) by in situ hybridization with riboprobes. Both PTHrP and its receptor messenger RNAs (mRNAs) were expressed not only in the skeleton, but also in many fetal extraskeletal tissues, such as choroid plexus, ears, lungs, tooth buds, heart, and skin. In these extraskeletal tissues PTHrP mRNA was expressed mainly in surface-lining cells, whereas its receptor mRNA was expressed mainly in adjacent mesenchyma cells. In endochondral bones, these two genes were expressed in largely discrete, but mostly neighboring, areas, although the localizations of these two mRNAs changed over developmental stages. The expression patterns of PTHrP and its receptor mRNAs during fetal development suggest PTHrP's roles as a paracrine factor and its involvement in epithelial-mesenchymal(-like) interactions.

Animals↗

PubMed2002

Expression during rat fetal development of GLUT12--a member of the class III hexose transporter family.

Glucose is an essential molecule for most mammalian cells, and is particularly important during fetal development, when cells are rapidly dividing and differentiating. In rats, GLUT1 is present at high levels in most fetal tissues, with levels decreasing after birth. We used immunohistochemistry to localise GLUT12 protein, a recently identified member of the sugar transporter family, and GLUT1 during rat fetal development. GLUT12 staining was observed in heart muscle from gestational days 15 to 21. GLUT12 staining in skeletal muscle increased from gestational days 17 to 21, and GLUT12 was also detected in brown adipose tissue. The expression of GLUT12 in insulin-responsive tissues supports a potential role for GLUT12 in the provision of glucose to these tissues before the appearance of GLUT4. GLUT12 protein was also expressed in fetal chondrocytes from gestational day 15 onward, in kidney distal tubules and collecting ducts from day 19, and in lung bronchioles from day 19. The specific pattern of expression observed in the rat fetus suggests that GLUT12 may be important in hexose delivery to developing tissues.

Animals↗

PubMed2006

Recombinant human follicle-stimulating hormone alters maternal ovarian hormone concentrations and the uterus and perturbs fetal development in mice.

Gonadotropins are routinely administered to produce multiple oocytes for clinical in vitro fertilization (IVF) treatment, laboratory research, and livestock industries. Studies in mice have shown gonadotropin stimulation using equine chorionic gonadotropin (eCG) affects the endometrium, implantation, and fetal development. Evidence from clinical studies also indicates that stimulation with recombinant human follicle-stimulating hormone (rhFSH) may be detrimental to the endometrium and implantation rates. We investigated the effect of rhFSH in mice on maternal plasma hormone concentrations and uterine gene and protein expression and the effect of a stimulated maternal environment on pregnancy. Adult females were stimulated with rhFSH or eCG, followed by human chorionic gonadotropin (hCG). On day 4 of pseudopregnancy, mice either had embryos transferred to the uterus or were killed, and blood and uterine samples were collected. Pregnancy outcomes were examined on day 15. Gonadotropin stimulation increased plasma progesterone concentrations on day 4 compared with controls, whereas estradiol concentrations were unaffected. Stimulation also reduced uterine leukemia inhibitory factor (Lif) mRNA, but the expression of estrogen and progesterone receptors (Esr1 and Pgr), homeobox gene Hoxa10, and Vegf mRNA were unchanged. Furthermore, distribution of uterine PGR protein expression was altered by stimulation, but LIF protein was unchanged. Stimulated embryo transfer recipients had lower pregnancy rates than controls, and fetuses from the rhFSH group had reduced weight, length, and maturity. These results demonstrate that gonadotropin stimulation with rhFSH or eCG alters the preimplantation maternal environment, which results in reduced pregnancy rates and fetal development in the mouse.

Animals↗

PubMed1999

Maternal dietary choline availability alters mitosis, apoptosis and the localization of TOAD-64 protein in the developing fetal rat septum.

Maternal changes in dietary choline availability alter brain biochemistry and hippocampal development in the offspring resulting in lifelong behavioral changes in the offspring. In order to better understand the relationship between maternal diet, brain cytoarchitecture and behavior, we investigated the effects of choline availability on cell proliferation, apoptosis and differentiation in the fetal rat brain septum. Timed-pregnant rats on day E12 were fed AIN-76 diet with varying levels of dietary choline for 6 days. We found that choline deficiency (CD) significantly decreased the rate of mitosis in the progenitor neuroepithelium adjacent to the septum. In addition, we found an increased number of apoptotic cells in the septum of CD animals compared to controls (3.5+/-0.5 vs. 1.7+/-0.5 apoptotic cells per section; p<0.05). However, CD had no effect on apoptosis in the indusium griseum (IG), a region of cortex dorsal to the septum. Using an unbiased image analysis method and a monoclonal antibody we found a decreased expression of the TOAD-64 kDa protein, a marker of commitment to neuronal differentiation during fetal development, in the dorsal lateral septum of CD animals. CD also decreased the expression of TOAD-64 kDa protein in the IG and cortical plate adjacent to the septum. These results show that dietary choline availability during pregnancy alters the timing of mitosis, apoptosis and the early commitment to neuronal differentiation by progenitor cells in regions of the fetal brain septum, as well as hippocampus, two brain regions known to be associated with learning and memory.

Animals↗

PubMed2006

Presence of SERCA and calcineurin during fetal development of porcine skeletal muscle.

Mechanisms involved in skeletal myofiber differentiation during fetal development of large animals are poorly understood. Studies in small animals suggest that the calcineurin (Cn) pathway is involved in myofiber differentiation. Neural activity is a prerequisite for Cn activity, implying maintenance of sustained low intracellular Ca(2+) concentrations. To study the role of Cn in fetal myofiber differentiation, we monitored the temporal and spatial distribution of Cn subunits, sarcoplasmic reticulum Ca(2+) ATPase (SERCA), phospholamban (PLB), and myosin heavy chain (MyHC) isoforms in relation to ingrowing nerves in porcine semitendinosus muscle (m. semitendinosus) at 55 and 75 days of gestation (dg) and at term. Immunofluorescence analysis revealed the presence of Cn subunits and SERCA isoforms at all analyzed stages. Cn distribution was not fiber-type specific, but expression became more prominent at term. At 75 dg, differential SERCA2 expression was accompanied by perinuclear PLB in primary fibers. SERCA1 was expressed in all fiber types at all stages. No specific MyHC isoform distribution was seen in relation to neuromuscular contacts, although neuromuscular contacts were present. From these results we speculate that in porcine m. semitendinosus differential SERCA2 expression precedes differential Cn expression. The question whether the Cn pathway is involved in prenatal myofiber differentiation needs further studies.

Animals↗

PubMed1998

Three-dimensional ultrasonographic assessments of fetal development.

OBJECTIVE: To visualize fetal surface anatomic structures in advancing gestation by use of three-dimensional ultrasonography with a specially developed abdominal three-dimensional transducer. METHODS: One hundred six normal fetuses from 9 to 40 weeks' gestation were studied with a specially developed abdominal three-dimensional transducer (3.5 MHz). This imaging system can provide conventional two-dimensional ultrasonography images and also can generate within seconds high-quality three-dimensional images in the surface and transparent modes with no need for an external workstation. We determined percentage of surface anatomic structures visualized at each trimester using two-dimensional and three-dimensional ultrasonography. RESULTS: The number and the clarity of surface anatomic structures increased from the first to the third trimester of pregnancy. The image quality was less distinct in the first trimester because of the small fetal size. The ability to view the fetal face, hands, and feet was better with three-dimensional ultrasonography than with two-dimensional ultrasonography in the first trimester (P < .05), whereas fetal genitals were viewed better with two-dimensional ultrasonography than with three-dimensional ultrasonography in the second and third trimesters (P < .05). CONCLUSION: Three-dimensional ultrasonography provides a new means of visualizing surface anatomic structures of the fetus in utero. Our results suggest that three-dimensional ultrasonography has the potential to be a supplement to two-dimensional ultrasonography and should be useful in evaluating fetal abnormalities in high-risk pregnancies.

Embryonic and Fetal Development↗

PubMed1988

The effect of campylobacter lipopolysaccharide on fetal development in the mouse.

Purified lipopolysaccharide (LPS) obtained from isolates of Campylobacter fetus ss. fetus and Campylobacter jejuni impaired fetal development when administered to mice on day 13 of pregnancy. Strikingly more fetal resorption was produced by C. jejuni LPS than by similar amounts of C. fetus ss. fetus LPS. Three of the four Campylobacter strains examined produced LPS that had no effect on maternal health, but LPS from one C. jejuni strain killed all of the mice to which it was administered.

Animals↗

PubMed1998

Effects of low-frequency magnetic fields on fetal development in CBA/Ca mice.

Effects of alternating magnetic fields (MFs) on the embryonic and fetal development in CBA/Ca mice were studied. Mated females were exposed continuously to a sinusoidal 50 Hz (13 microT or 0.13 mT root mean square) or a sawtooth 20 kHz (15 microT peak-to-peak) MF from day 0 to day 18 of pregnancy for 24 h/day until necropsied on day 18. Control animals were kept under the same conditions without the MF. MFs did not cause maternal toxicity. No adverse effects were seen in maternal hematology and the frequency of micronuclei in maternal bone marrow erythrocytes did not change. The MFs did not increase the number of resorptions or fetuses with major or minor malformations in any exposure group. The mean number of implantations and living fetuses per litter were similar in all groups. The corrected weight gain (weight gain without uterine content) of dams, pregnancy rates, incidences of resorptions and late fetal deaths, and fetal body weights were similar in all groups. There was, however, a statistically significant increase in the incidence of fetuses with at least three skeletal variations in all groups exposed to MFs. In conclusion, the 50 Hz or 20 kHz MFs did not increase incidences of malformations or resorptions in CBA/Ca mice, but increased skeletal variations consistently in all exposure groups.

Animals↗

PubMed1993

Treatment with gonadotropins impaired implantation and fetal development in mice.

PURPOSE: The effect of gonadotropins on implantation and fetal development in mice was investigated by superovulation with pregnant mare serum gonadotropin and human chorionic gonadotropin. In a previous study fetal growth was found to be highly retarded. RESULTS: Assessment of implantation in vivo revealed that late implantation did occur. Gestational length was highly extended, the mean number of live fetuses per pregnant mouse was lower and their mean weight significantly reduced. In vitro experiments revealed no significant difference in the rate of blastocyst adhesion and trophoblast outgrowth development. Immunohistochemical staining, however, showed that blastocysts from superovulated mice had smaller trophoblastic outgrowths than control embryos. Staging embryonic development at the time of flushing, however, revealed retarded embryo development in vivo in hormone-treated mice. After correlation with embryonic stage at the beginning of the culture, there was no difference in the size of trophoblastic outgrowths. CONCLUSION: Treatment with gonadotropins impaired implantation and embryonic/fetal development. Changes in maternal milieu, rather than in embryo quality, may be responsible for the adverse effects observed.

Animals↗

PubMed2003

Fetal development of the segment-specific papillary body in the equine hoof.

Fetal development of the unique papillary body and its localized peculiarities in the equine hoof are described based on the study of 51 fetuses, nine newborn foals, and five adult horses. The shape and dimensions of the dermal papillae and lamellae have a formative influence on the structure and physical quality of the corneous hoof capsule with its horn tubules and lamellae. The size and arrangement of these horn structures determine the mechanical quality of hoof horn. Proper horn quality is a prerequisite for the various functions of the hoof capsule, such as protecting the living dermis supporting the hoof capsule, shock absorption, and formation of the suspensory apparatus of the distal phalanx. Development of the segment-specific papillary body is initiated by the increasing mitotic activity of the epidermal cells invaginating the dermal surface, thus forming dermal microridges. These microridges are transformed into single dermal papillae, which are arranged in rows, or enlarged to become primary and secondary dermal lamellae. The formation of a segment-specific papillary body enables the increasing keratinization ratio in the hoof epidermis and the formation of the characteristic tubular and lamellar horn responsible for the special mechanical properties of hoof horn.

Animals↗

PubMedDate not supplied

Fetal development in alloxan-treated rats.

The effect of alloxan on embryo and fetal development in rats was evaluated. Alloxan was injected intraperitoneally (ip) in pregnant rats at doses of 80 to 150 mg/kg at Day 0 (day of fertilization), and 110 mg/kg at Day 4 of pregnancy. Hyperglycemia was rarely produced at alloxan doses from 80 to 100 mg/kg, and the frequency of malformations observed was low. Higher doses (110 to 150 mg/kg) caused severe hyperglycemia, and maternal or embryonic death. When 110 mg/kg was administered on Day 4 of gestation (the day before embryo implantation), all rats had resorption nodules and litters with embryos with delayed growth. We recommend the induction of diabetes mellitus on Day 4 of pregnancy for studies of diabetes-gestation interaction.

Alloxan↗

PubMed1999

The effects on fetal development of high alpha-fetoprotein and maternal smoking.

OBJECTIVES: This study determined the risk of impaired fetal growth resulting from the interaction between maternal smoking during pregnancy and unexplained elevated concentrations of maternal serum alpha-fetoprotein (MSAFP). METHODS: This observational study involved 123 pregnant smokers with unexplained second-trimester elevated concentrations of MSAFP, 827 smokers with normal levels, and 471 nonsmokers with raised levels. RESULTS: By logistic regression, coincident smoking and elevated MSAFP levels were found to be associated with increases in the low basic risks of prematurity, small-for-gestational-age births, low birthweight, and need for neonatal care. CONCLUSIONS: Maternal smoking has an adverse effect on fetal development in pregnancies with unexplained elevated MSAFP concentrations. Such pregnancies merit close surveillance.

Adult↗

PubMed1983

Estrogen and antiestrogen effects on different lymphoid cell populations in the developing fetal thymus of guinea pig.

Estrogen responsiveness in the developing fetal thymus of guinea pig has been investigated. One-day estradiol (E2) treatment (1 mg/kg BW) of pregnant animals selectively decreases the number of larger lymphoid cells of the outer cortex of the fetal thymus, without affecting the global number of cortical lymphocytes. E2 treatments for longer periods (from 2 until 6 days) provoke a further impairment in the pattern of outer cortical lymphocytes, selectively reducing larger lymphoid cells, and also decrease the global number of cortical lymphocytes without affecting medullary lymphocytes. Treatment with the antiestrogen tamoxifen (2 mg/kg BW . day for 6 days) results in a transfer of cytoplasmic estrogen receptor to the nuclei of fetal thymus and also affects the histology of the fetal organ, although to a lesser extent than E2. However, when tamoxifen is administered with E2 (1 mg/kg BW . day during the last 3 days of tamoxifen treatment), it antagonizes all of the effects induced by E2 alone on the fetal thymus. The 6-day E2 treatment decreases the weight of the fetal thymus in an age-dependent manner; this effect is progressively more intense from 42 days of gestation at the time of treatment (mean +/- SE, 25 +/- 5% decrease) up to the end of gestation (63 +/- 7% decrease). The effect of E2 on large lymphoid cells also increases in an age-dependent manner. The extent of the estrogen responses observed is correlated with the levels of cytoplasmic estrogen receptors, which increase from 38 days to the end of gestation. The intracellular compartmentalization of estrogen receptor shows that cytoplasmic estrogen receptors are transferred to the nuclei by E2 at both younger and older ages. It is concluded that E2 has differential actions on the lymphoid cell population of the fetal thymus of guinea pig by events antagonized by the antiestrogen tamoxifen and related to the availability and development of cytoplasmic estrogen receptors.

Animals↗

PubMed2002

The role of growth hormone in fetal development.

Studies across several species, particularly the mouse, show that growth hormone (GH, somatotrophin) is an important determinant of litter size, and to a lesser extent, of birth length. GH acts at all stages of development, from ovulation through preimplantation development to the late fetus, with actions on both embryo/fetus and mother contributing to successful fetal development. The fact that these are not more obvious in vivo is likely a result of redundancy of cytokine hormone action, particularly in relation to prolactin, which shares common actions and receptor locations with GH.

Animals↗

PubMed1992

Distribution of osteonectin mRNA and protein during human embryonic and fetal development.

We investigated the temporal and spatial distribution of osteonectin during human embryonic and fetal development, using in situ hybridization and immunohistochemistry. Osteonectin gene expression was generally found in cells exhibiting high rates of matrix production/proliferation. In mineralized tissue, a strong signal was obtained in osteoblasts, odontoblasts, and chondrocytes of the upper hypertrophic and proliferative zones. Chondrocytes of the mineralized zone showed no expression throughout the different stages of development. Strong osteonectin expression was found in odontoblasts of developing teeth. In addition, osteonectin mRNA and protein were detected in several non-mineralized tissues: steroid-producing cells of the adrenal gland and the gonads, kidney (glomeruli), lung (bronchi), skin, megacaryocytes, and large vessels. Histochemistry confirmed the results and detected extracellular osteonectin in bone and in the zone of mineralized cartilage only. The localization of osteonectin in bone, cartilage, and teeth is consistent with a role in the initiation of mineralization. However, the organ-specific distribution in non-mineralized tissues suggests an important multifunction role of this protein during human development.

Abortion, Spontaneous↗