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PubMed1999

Paralogous mouse Hox genes, Hoxa9, Hoxb9, and Hoxd9, function together to control development of the mammary gland in response to pregnancy.

Although the role of Hox genes in patterning the mammalian body plan has been studied extensively during embryonic and fetal development, relatively little is known concerning Hox gene function in adult animals. Analysis of mice with mutant Hoxa9, Hoxb9, and Hoxd9 genes shows that these paralogous genes are required for mediating the expansion and/or differentiation of the mammary epithelium ductal system in response to pregnancy. Mothers with these three mutant genes cannot raise their own pups, but the pups can be rescued by fostering by wild-type mothers. Histologically, the mammary glands of the mutant mothers seem normal before pregnancy but do not develop properly in response to pregnancy and parturition. Hoxa9, Hoxb9, and Hoxd9 are expressed normally in adult mammary glands, suggesting a direct role for these genes in the development of mammary tissue after pregnancy. Because loss-of-function mutations in these Hox genes cause hypoplasia of the mammary gland after pregnancy, it may be productive to look for misexpression of these genes in mammary carcinomas.

Animals↗
PubMed1993

Spatial and temporal distribution of corticosteroid-binding globulin and its messenger ribonucleic acid in embryonic and fetal mice.

Glucocorticoids influence fetal development, and their actions are regulated by plasma corticosteroid-binding globulin (CBG). Immunohistochemistry and in situ hybridization were, therefore, used to localize CBG and its mRNA in sections of embryonic and fetal mice and their associated placental tissues from day 5 of gestation until term (day 19). In the fetus, CBG mRNA was first detectable in the hepatocytes on day 11 of gestation. The amount of CBG mRNA in these cells increased transiently to a maximum on days 15-16 of gestation and was negligible by day 19. In hepatocytes, CBG immunoreactivity correlated with the distribution and relative abundance of CBG mRNA. The fetal exocrine pancreas also contained CBG mRNA, but this was only present on days 15-16 of gestation, while immunoreactive CBG persisted in these cells until term. Immunoreactive CBG was detected in the tubular cells of the developing fetal kidney as early as day 13, but CBG mRNA was never found in the fetal kidney, suggesting that the protein is probably sequestered from fetal blood directly or via the glomerular filtrate. The placenta contained immunoreactive CBG throughout gestation, even before its detection in fetal tissues, and it was most abundant in the spongiotrophoblasts and the extracellular matrix surrounding fetal and maternal capillaries. However, CBG mRNA was not detected in the placenta at any gestational age. Therefore, CBG present in the placenta is most likely of maternal origin and may influence the activities of steroid hormones that control placental development and/or function. The presence of smaller immunoreactive polypeptides in placental extracts, compared to CBG in corresponding maternal serum samples, suggests that this process may involve an interaction between maternal CBG and placental proteinases. The results presented here suggest that temporal and spatial changes in the localization of CBG and its mRNA in the fetus may influence the effects of steroid hormones on developing tissues.

Amino Acid Sequence↗
PubMed1987

Evaluation of the effects of inhalation exposure to 1,3-dichloropropene on fetal development in rats and rabbits.

1,3-Dichloropropene (DCP), which has found widespread use as a soil fumigant, was evaluated for its potential effects on embryonal and fetal development in rats and rabbits. Pregnant Fischer 344 rats and New Zealand White rabbits were exposed to 0, 20, 60, or 120 ppm of 1,3-dichloropropene for 6 hr/day during gestation Days 6-15 (rats) or 6-18 (rabbits). Exposure-related decreases in maternal weight gain and feed consumption were observed in rats at all treatment levels. Decreased weight gain was also observed among rabbits at 60 and 120 ppm. A slight, but statistically significant, increase in the incidence of delayed ossification of the vertebral centra in rats exposed in utero to 120 ppm of DCP was considered of little toxicologic significance in light of the maternal toxicity observed at this exposure concentration. No evidence of a teratogenic or embryotoxic response was observed in either species at any exposure level tested. Thus, it was concluded that DCP was not teratogenic at exposure levels up to 120 ppm in either rats or rabbits.

Aerosols↗
PubMed1990

Smooth muscle actin expression during rat gut development and induction in fetal skin fibroblastic cells associated with intestinal embryonic epithelium.

Cytodifferentiation of smooth muscle cells has been analyzed immunocytochemically during rat intestinal development and in chimaeric intestines by using monoclonal antibodies reacting specifically with smooth muscle actin species (CGA7 [10] and anti-alpha SM-1 [40]). As development proceeds, the various intestinal muscle layers differentiate in the following order: (1) cells expressing smooth muscle actin appear within the mesenchyme of the 15-day fetal rat intestine, in the circular muscle-forming area, the differentiation of cells in the presumptive longitudinal muscle layer starting with a 48-h delay; (2) smooth muscle fibers appear within the connective tissue core of the villi shortly after birth, in parallel with a progressive formation of the muscularis mucosae, which becomes clear-cut only in the course of the 2nd week after birth; (3) a distinct cell layer in the innermost part of the circular muscle layer arises during the perinatal period. Thereafter, the fluorescence pattern remains unchanged until the adult stage. Chimaeric intestines were constructed by the association of 14-day fetal intestinal epithelium and cultured fetal rat or human skin fibroblasts. These fibroblastic cells did not express actin at the time at which they were associated. The immunocytochemical analysis of smooth muscle actin in the hybrid intestines, which had developed as intracoelomic grafts for 12 days, revealed that the skin fibroblastic cells had been induced by the intestinal epithelial cells to differentiate into smooth muscle cells. Such a result was also obtained with allantoic endoderm. It was not obvious in cocultures of intestinal epithelium with skin fibroblastic cells. However, when intestinal epithelial cells were cocultured with intestinal mesenchymal cells, actin expression was stimulated in the latter cell population.

Actins↗
PubMed1996

Endogenous retinoic acid signaling colocalizes with advanced expression of the adult smooth muscle myosin heavy chain isoform during development of the ductus arteriosus.

During fetal development, a specialized vessel the ductus arteriosus, shunts blood from the pulmonary artery to the aorta, thus bypassing the lungs. The ductus differs primarily from the great vessels in that it is a muscular rather than an elastic artery, and the etiology of this differential development remains controversial. We present evidence that retinoic acid (RA) may contribute to the unique muscle phenotype of the ductus arteriosus. Using a transgenic mouse carrying an RA response element-lacZ transgene that expresses beta-galactosidase (beta-gal) in response to endogenous RA signals during embryonic and fetal development, we observe a strong beta-gal signal in the ductus arteriosus. By immunofluorescence, this signal colocalizes with the expression of the adult-specific smooth muscle myosin heavy chain isoform, SM2. The beta-gal signal is present throughout fetal development and persists in the neonate until the ductus arteriosus is completely closed. beta-Gal-positive cells are first detected by immunofluorescence at 13.5 days postcoitum (dpc) in the mesenchyme surrounding the ductus. By 15.5 dpc, very intense beta-gal staining localizes to the ductus arteriosus but is absent or minimal in the pulmonary trunk and aortic arch; by 17.5 dpc, the smooth muscle layers of the tunica media in the ductus arteriosus exhibit positive beta-gal staining. Immunostaining with antibodies against smooth muscle myosins shows that, while SM1 is expressed in all embryonic vessels, SM2 is precociously expressed in the ductus arteriosus. Furthermore, SM2 expression can be detected in the ductus as early as 15.5 dpc. In the neonate, the beta-gal signal persists in the smooth muscle layer of the ductus and immunostaining colocalizes with SM2 expression. These data suggest that RA may play a role in inducing and maintaining smooth muscle differentiation in the developing ductus arteriosus and may promote precocious expression of the adult vascular phenotype.

Animals↗
PubMed1995

Expression of gap junction genes, connexin40 and connexin43, during fetal mouse development.

The expression patterns of the gap junction genes connexin40 and connexin43 have been analyzed during late mouse fetal development, i.e., at embryonic days 14.5 and 16.5, by in situ hybridization and immunofluorescence. Connexin40 was found in endothelial cells of vessels, cardiomyocytes and in developing myoblasts and myotubes. Expression of connexin40 in developing muscle fibers was strong in the back muscles and weaker in the muscles of the limbs. The number of labeled cells in the back muscle decreased with ongoing differentiation of myoblasts, in accordance with the idea that connexin40 is only expressed in the early stages of muscle cell differentiation. Within a muscle bundle, connexin40 expression was predominantly found at the outermost side where myoblasts fuse to multinucleated myotubes. In contrast, connexin43 exhibits a wide and complex pattern of expression in fetal mouse development. It is found in organs originating from all three germ layers, such as epidermis, heart, lung, muscle, kidney and gut. Connexin43 transcript and protein were very abundant in tissues that had been undergoing inductive interactions, e.g., the inner enamel epithelium of the teeth, the glomeruli of the kidneys and the infundibulum forming the neural part of the pituitary gland. Very high connexin43 expression was found in the embryonic meninges (dura mater) and in the fetal adrenal cortex. During keratinocyte differentiation connexin43 mRNA expression decreased, being much stronger in the stratum basale than in stratum granulosum. No obvious discrepancy between the amount of mRNA and protein of either connexin was noticed, suggesting that there is no specific translational regulation at these developmental stages.

Animals↗
PubMed1989

The developing neuroepithelium in human embryonic and fetal brain studied with vimentin-immunocytochemistry.

The neuroepithelial cells, which constitute the primordium of the CNS, are potentially capable of generating neuronal and glial cell lineages concomitantly. The appearance and morphological development of vimentin-positive neuroepithelial cells in human embryonic and fetal brain (4-16 weeks) were studied with immunocytochemistry. In embryos aged 4-6 weeks, vimentin-reactivity was seen in all neuroepithelial cells, including those which exhibited mitotic figures. The distribution of reactivity changed according to a general developmental pattern, which commenced and proceeded temporally different in various regions of the CNS. All regions exhibited vimentin-positive neuroepithelial cells, the distribution and morphology of which gradually changed, resulting in lamination of the neural wall into two and subsequently three layers. The neocortex and midline raphe were the only regions to differ significantly from the general pattern. When reactivity to glial fibrillary acidic protein developed at 7-8 weeks, the distribution was very much like that of vimentin at the same stage. Reactivity to glial, neuronal and other cellular markers (S-100, neurofilament, neuron specific enolase, desmin, and cytokeratin) revealed different distributions. Although cells retaining vimentin beyond the ventricular zone stage are radial glial cells and presumptive fibrous astrocytes, it seems unlikely that vimentin is a marker for a distinct cell lineage during early CNS development. It is suggested that all neuroepithelial cells in vivo differentiate to a stage where they express vimentin, and that vimentin may have a functional role in cellular movements and during the interkinetic nuclear migration.

Antibodies, Monoclonal↗
PubMed2003

Role of the hepatocyte nuclear factor 4alpha in control of the pregnane X receptor during fetal liver development.

The fetal liver, the major site of hematopoiesis during embryonic development, acquires additional functions near birth. Among the important liver functions is the response to xenobiotic exposure due to expression of several cytochromes P450 (CYP) and drug efflux transporters. Expression of these genes is regulated by nuclear receptors such as the pregnane X receptor (PXR). In this study, regulation of xenobiotic responses during fetal liver development was analyzed using a fetal hepatocyte primary culture system derived from embryonic day 15 (E15) livers. Hepatocyte nuclear factor (HNF) 4alpha regulates the expression of many genes preferentially in the liver. Expression of several xenobiotic response genes as well as HNF4alpha was increased in fetal hepatocytes stimulated by the hepatic maturation factors oncostatin M (OSM) and Matrigel. To determine the contribution of HNF4alpha to xenobiotic responses in the fetal liver, fetal hepatocytes containing floxed HNF4alpha alleles were cultured and the HNF4alpha gene was inactivated by infection with an adenovirus containing the Cre gene. Expression of CYP3A11 and PXR was suppressed by inactivation of HNF4alpha. An HNF4alpha binding site was characterized in the PXR promoter and found to be required for activation of the PXR promoter in fetal hepatocytes. In conclusion, HNF4alpha is the key transcription factor regulating responses to xenobiotics through activation of the PXR gene during fetal liver development.

Animals↗
PubMed2000

Mouse submandibular gland morphogenesis: a paradigm for embryonic signal processing.

Signal processing is the sine qua non of embryogenesis. At its core, any single signal transduction pathway may be understood as classic Information Theory, adapted as an open system such that, because of networking, the "receiver" is presented with more information than was initially signaled by the "source". Over 40 years ago, Waddington presented his "Epigenetic Landscape" as a metaphor for the hierarchical nature of embryogenesis. Mathematically, Waddington's landscape may be modeled as a neural net. The "black box" of the neural net is an interacting network of signal transduction pathways (using hormones, growth factors, cytokines, neurotransmitters, and others) which inform the Boolean logic gates. An emerging theme in developmental biology is that defined sets of epigenetic circuits are used in multiple places, at multiple times, for similar and sometimes different purposes during organogenesis. As we show here, submandibular gland embryonic and fetal development is a splendid paradigm of these epigenetic circuits and their phenotypic outcomes, such as branching and lumen formation.

Animals↗
PubMed1991

Karyotypes and X chromosome inactivation in segregants of a murine X-autosome translocation, T(X;4)37H.

Karyotypes and X chromosome inactivation were studied in embryos obtained from female mice carrying T(X;4)37H translocation on day 6 to 8 of gestation by a BrdU-acridine orange method. A total of 18 different karyotypes were found in 477 embryos examined: 90.0% embryos were products expected from 2:2 alternate or adjacent 1 disjunction. 3:1 and adjacent 2 disjunctions accounted for approximately 8.0% and 0.7% conceptuses, respectively. In the embryo proper of balanced T37H/ + conceptuses, inactivation was random with respect to the normal X and the larger translocation X (4x) chromosome. In all the cells with the 4x inactive, the late replication apparently did not spread to the attached autosomal portion, although black/brown coat variegation implies spreading of inactivation into the autosomal region. The X chromosome segment deprived of the inactivation center remained active in all the cells examined and it exerted deleterious effects on embryonic or fetal development. Observation in embryos having two maternally derived X chromosomes showed that they were indeed resistant to inactivation in early extraembryonic cell lineages, and two copies of active X chromosomes in the trophectoderm fatally affected embryonic development due to inability to form the extraembryonic ectoderm and ectoplacental cone from the polar trophectoderm. In unbalanced X aneuploids the X chromosomes with the deletion were preferentially inactivated due to strong selection against nullisomy X.

Animals↗
PubMed2006

Investigations of a human embryonic globin gene silencing element using YAC transgenic mice.

A silencing element has been previously located upstream of the human epsilon-globin gene promoter using transient assays and transgenic mice carrying plasmid constructs in which the element has been deleted or its transcriptional motifs have been mutated. To investigate whether this element functions in the context of the whole beta-globin locus, we analyzed epsilon-globin gene expression in transgenic mice carrying a deletion of the silencing element in the context of a 213-kilobase human beta-globin yeast artificial chromosome (beta-YAC). epsilon-Globin gene expression was measured during embryonic and fetal development and in adult mice. epsilon-mRNA levels in embryonic cells in Day 12 blood were as high as those measured in wild-type beta-YAC controls, indicating that the deletion does not affect epsilon gene promoter function. epsilon-Globin gene expression was confined to the embryonic cells, indicating that deletion of this silencing element did not affect epsilon-globin developmental expression in the context of the beta-YAC. These results suggest that in the context of the whole beta-globin locus, other proximal and upstream epsilon gene promoter elements as well as competition by the downstream globin genes contribute to the silencing of the epsilon-globin gene in the cells of definitive erythropoiesis.

Animals↗
PubMed1994

Septation of the respiratory and digestive tracts in human embryos: crucial role of the tracheoesophageal sulcus.

Esophageal atresia and tracheoesophageal fistula, common malformations of the respiratory and digestive tracts, are of unsettled pathogenesis. Part of the difficulty in understanding these abnormalities arises from the uncertainties about the normal developmental processes in the region. This study examined the development and fate of the tracheoesophageal septum. Normal human embryos from the Carnegie Embryological Collection and fetuses from the Hopkins Pathology Collection were examined, and reconstructions of selected specimens were made from photomicrographs of serial histologic sections. The results show that the lung bud appears in Carnegie stage 12, rapidly enlarges, and bends caudally, thereby producing a sulcus between the foregut and the respiratory system on its caudal aspect. The cranial aspect of this tracheoesophageal sulcus remains fixed at the levels of the first cervical vertebra throughout subsequent embryonic and fetal development. At the same time the trachea and esophagus elongate to bring those part of the respiratory and digestive systems into their definitive anatomic positions. Examination of the tracheoesophageal sulcus shows that its growth-limiting properties may be explained by its catenoidal configuration. Catenoidal, or saddle-shape, sulci have been shown to have similar regional growth-limiting properties in the embryonic heart. These regions contrast with outwardly convex regions in both the developing heart and lung where growth of the tissues occurs. The observations made here suggest that the origin of the tracheoesophageal malformations must be sought in a configurational abnormality in the area of the developing lung bud in Carnegie stage 12.

Digestive System↗
PubMed1998

Growth hormone: a paracrine growth factor in embryonic development?

Although pituitary growth hormone is obligatory for normal postnatal growth and development, early embryonic and fetal growth is generally considered to be independent of pituitary GH. Indeed, in chickens, somatotrophs and serum GH are not detectable until late in embryogenesis, and neither partial decapitation nor pre-hatch GH administration greatly affects embryonic growth. However, since it is now known that GH can be produced and act in many extra-pituitary tissues, early embryonic growth may be independent of pituitary GH but dependent upon the paracrine actions of extra-pituitary GH. The possibility that growth hormone may be a paracrine growth factor during early development will therefore be considered in this brief review, which is based on the embryogenesis of the domestic fowl.

Animals↗
PubMed2004

Vitamin a requirement for early cardiovascular morphogenesis specification in the vertebrate embryo: insights from the avian embryo.

Vitamin A is required throughout the life cycle, including crucial stages of embryonic and fetal development. With the identification of retinoic acid-specific nuclear transcription factors, the retinoid receptors, considerable advances have been made in understanding the molecular function of vitamin A. The requirement for vitamin A during early embryogenesis has successfully been examined in the vitamin A-deficient avian embryo during neurulation, when in the vertebrates crucial developmental decisions take place. These studies revealed that retinoic acid is essential during these early stages of embryogenesis for the initiation of organogenesis (i.e., formation of the heart). If retinoic acid is not present at this time, abnormal development ensues, leading to early embryonic death. Though the initial insult of the absence of vitamin A appears to be on the specification of cardiovascular tissues, subsequently all development is adversely affected and the embryo dies. Molecular and functional studies revealed that retinoic acid regulates the expression of the cardiogenic transcription factor GATA-4 and several heart asymmetry genes, which explains why the heart position is random in vitamin A-deficient quail embryos. During the crucial retinoic acid-requiring developmental window, retinoic acid transduces its signals to genes for heart morphogenesis via the receptors RARalpha2, RARgamma, and RXRalpha. Elucidation of the function of vitamin A during early embryonic development may lead to a better understanding of the cardiovascular birth defects prevalent in the Western world.

Animals↗
PubMed2001

Quantitative immunohistochemical analysis of the expression of CD31 during lung development in the rat.

The CD31 antigen, known also as the platelet/endothelial cell adhesion molecule 1, has been shown to be a good marker for monitoring the formation of the vasculature in mammals. Available evidence suggests that the expression of CD31 is regulated during embryonal and fetal development. The aim of the present study was to evaluate the changes in the expression of CD31 during the development of the rat lung. We studied samples of lung tissue from rat fetuses (17, 19 and 21 days after conception), newborns (1, 3, 5, 7, 14 and 21 days after birth) and adult animals. The tissue samples from rats in the various age groups were divided into sets, with all age groups being represented in every set. After immunohistochemical localization of the antigen, the amount of chromogen deposited after the immunoreaction (defined in terms of optical density; OD) was evaluated by image analysis in the various sets. Measurements were obtained twice from each set, and the results were reproducible (paired t test, alpha = 0.05). We subjected the results of measurements from all sets to an analysis of variance (ANOVA). The amount of chromogen (OD) decreased from fetal day 19 to 5 days after delivery and then increased again. The decrease in the level of expression of CD31 on days 3 and 5 after delivery was significant (p < 0.0001).

Animals↗