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Results for “Embryonic Structures”

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At least 271 records · Page 15Linked to original sources

PubMed2004

A right-sided aortic arch misdiagnosed as asthma since childhood.

Congenital malformation of the aortic arch complex occurs in 3% of humans. These vascular aberrations result from embryonic structures that persist when there is incomplete atrophy or regression during normal development. Typically, anomalies of the aortic arch do not cause respiratory symptoms. However, in some individuals, the unusual position of the remnant vessels may compress the airway and cause airflow limitation. As might be expected, a symptomatic vascular anomaly is most often clinically apparent in childhood. We report an adult male with exertional dyspnea who had been diagnosed with asthma since childhood. After his symptoms proved refractory to newer asthmatic therapy, he was referred for further evaluation. Bronchial hyperactivity was not present with objective testing, and compression of his trachea by a right-sided aortic arch was confirmed with appropriate imaging studies. This report illustrates the need to confirm the diagnosis of asthma with objective measures of airflow and reminds the clinician that a congenital vascular aberrancy may initially elude diagnosis.

Aorta, Thoracic↗

PubMed1999

Differential function of N-cadherin and cadherin-7 in the control of embryonic cell motility.

Similar amounts of N-cadherin and cadherin-7, the prototypes of type I and type II cadherin, induced cell-cell adhesion in murine sarcoma 180 transfectants, Ncad-1 and cad7-29, respectively. However, in the initial phase of aggregation, Ncad-1 cells aggregated more rapidly than cad7-29 cells. Isolated Ncad-1 and cad7-29 cells adhered and spread in a similar manner on fibronectin (FN), whereas aggregated cad7-29 cells were more motile and dispersed than aggregated Ncad-1 cells. cad7-29 cells established transient contacts with their neighbors which were stabilized if FN-cell interactions were perturbed. In contrast, Ncad-1 cells remained in close contact when they migrated on FN. Both beta-catenin and cadherin were more rapidly downregulated in cad7-29 than in Ncad-1 cells treated with cycloheximide, suggesting a higher turnover rate for cadherin-7-mediated cell-cell contacts than for those mediated by N-cadherin. The extent of FN-dependent focal adhesion kinase phosphorylation was much lower if the cells had initiated N-cadherin-mediated rather than cadherin-7-mediated cell adhesion before plating. On grafting into the embryo, Ncad-1 cells did not migrate and remained at or close to the graft site, even after 48 h, whereas grafted cad7-29 cells dispersed efficiently into embryonic structures. Thus, the adhesive phenotype of cadherin-7-expressing cells is regulated by the nature of the extracellular matrix environment which also controls the migratory behavior of the cells. In addition, adhesions mediated by different cadherins differentially regulate FN-dependent signaling. The transient contacts specifically observed in cadherin- 7-expressing cells may also be important in the control of cell motility.

Animals↗

PubMed1998

The sella turcica in children with lumbosacral myelomeningocele.

The purpose of the present study was to analyze the morphology of the sella turcica in children born with myelomeningocele. Profile radiographs from 16 children (nine females and seven males) born with myelomeningocele were analysed. The contour of the anterior wall of the sella turcica in myelomeningocele patients, instead of following the normal cranio-caudal direction, was always in an obliquely antero-posterior direction. The sella turcica thus appeared broad cranially with a diverging anterior wall, or with both diverging anterior and posterior walls. This appearance gave and impression of a wide sella turcica in myelomeningocele with less depth than normal. The investigation has drawn attention to the fact that congenital malformations in the axial skeleton, even though, as in the case of myelomeningocele, they are located far from the cranial base, may have manifested themselves in the cranial base as well. The pathogenetic relationship between these manifestations is to be found in the early embryonic structure, the notochord. With the concept of embryological developmental fields, defined as areas with a common developmental origin, such as the notochordal field involved in myelomeningocele, new ways seem to be emerging for an improvement of aetiologically based diagnosis and treatment.

Adolescent↗

PubMed2003

Molecular mechanisms underlying limb anomalies associated with cholesterol deficiency during gestation: implications of Hedgehog signaling.

Human disorders caused by inborn errors of cholesterol biosynthesis are characterized by dysmorphogenesis of multiple organs. This includes limb malformations that are observed at high frequency in some disorders, such as the Smith-Lemli-Opitz syndrome, indicating a pivotal role of cholesterol in limb morphogenesis. Recently, it has been demonstrated that cholesterol can modulate the activity of the Hedgehog proteins, that act as morphogens to regulate the precise patterning of many embryonic structures, among which the developing limbs. To provide insight in the functions of cholesterol during limb development and in the potential role of Hedgehog signaling in the genesis of limb defects, we developed an in vivo rat model of cholesterol deficiency. We show here that treatment with Triparanol, a distal inhibitor of cholesterol biosynthesis, induced patterning defects of the autopod at high frequency, including pre-axial syndactyly and post-axial polydactyly, thus reproducing limb anomalies frequently observed in humans. Using in situ hybridization, we show that these malformations originate from a modification of Sonic Hedgehog signaling in the limb bud at 13 days post-coitum, leading to a deficiency of the anterior part of the limb. This deficiency results in an imbalance of Indian Hedgehog expression in the forming cartilage, ultimately leading to reduced interdigital apoptosis and syndactyly. Our study thus unravels the molecular mechanisms underlying the genesis of limb defects associated with cholesterol deficiency in rodents, and most probably in humans.

Animals↗

PubMed1991

A clinical, histological, and immunohistochemical comparison of acrodermatitis chronica atrophicans and morphea.

We compared 19 patients with acrodermatitis chronica atrophicans (ACA), a dermatosis caused by Borrelia burgdorferi infection, and 40 patients with morphea, a disease of heterogeneous origin where a borrelia etiology has been suggested in some cases, both clinically and histologically to define the differences between these two dermatoses. Clinically, ACA involves acral body sites with lower temperatures, is seen mostly in elderly persons, and presents as a livid discoloration that is not sharply demarcated. Morphea can be localized in embryonal structures, affects any age and body site, and exhibits extension at the periphery of the lesions. Histologically, ACA shows atrophy of collagen and elastic tissue as well as hypertrophic basophilic elastic tissue; whereas in morphea, sclerosis and polarizing elastic tissue are prominent. Graft-versus-host-like reactions may be present in both dermatoses. Immunohistochemical testing with different lymphocyte markers showed differences only in the expression of HLA-DR antigens. These conditions can be distinguished from each other on a clinical and histological basis in most cases. In 17% of morphea biopsy specimens, however, histological differentiation from ACA was not possible. Moreover, the histological pattern of morphea was not associated with a positive borrelia serology.

Acrodermatitis↗

PubMed2003

p63 expression in solid cell nests of the thyroid: further evidence for a stem cell origin.

Solid cell nests of the thyroid are embryonic remnants of endodermal origin that may be difficult to distinguish from squamous metaplasia, metastatic squamous carcinoma, papillary microcarcinoma, medullary carcinoma, and C-cell hyperplasia. These embryonic structures are composed of main cells and C-cells; cystic structures and mixed follicles are sometimes observed intermingled with solid cell nests. Recently, p63, a p53 homologue that is consistently expressed in basal/stem cells of stratified epithelia and plays a major role in triggering the differentiation of some specific cell lineages, has been characterized. We evaluated the immunohistochemical expression of p63, cytokeratins (CAM 5.2, AE1/AE3, 34betaE12, 7, and 20), carcinoembryonic antigen, thyroid transcription factor 1 (TTF-1), thyroglobulin, and calcitonin using the streptavidin-biotin-peroxidase complex technique in 6 bona fide solid cell nests. We observed that main cells of solid cell nests are strongly decorated by p63, while C-cells and all other thyroid structures were consistently negative. Moreover, main cells expressed carcinoembryonic antigen and all cytokeratins but cytokeratin 20 and lacked TTF-1, thyroglobulin and calcitonin. In contrast to this, C-cells of solid cell nests were immunoreactive for calcitonin, CAM 5.2, AE1/AE3, and cytokeratin 7; focal immunoreactivity for TTF-1 was also observed in some C-cells. We conclude that main cells of the solid cell nests display a basal/stem cell phenotype (p63 and basal cytokeratin positivity), whereas C-cells show features of parafollicular differentiation. We conclude, furthermore, that p63 antibodies may help in distinguishing solid cell nests from their mimics.

Adenoma↗

PubMed2025

Dual-patterned pluripotent stem cells self-organize into a human embryo model with extended anterior-posterior patterning.

Human gastruloids are a powerful class of stem cell-derived models that recapitulate key features of early embryonic development, including symmetry breaking and the emergence of three germ layers1-3. However, they lack anterior embryonic structures and coordinated axial organization4-6. To address this limitation, we pre-patterned human pluripotent stem cells (hPSCs) by exposing them to either anterior (FGF2) or posterior (CHIR99021 [CHIR] & retinoic acid [RA]) cues. Upon mixing, these dual-patterned hPSCs interacted and self-organized into elongated structures with both anterior and posterior features-which we term anterior-posterior (AP) human gastruloids. Anteriorly pre-treated cells robustly intercalated into posteriorly pre-treated cells, collectively giving rise to a continuum of neural tissues-including a brain-like domain, a neural tube-like structure, and neuro-mesodermal progenitors (NMPs)-with segmented somites arrayed bilaterally. Single cell RNA sequencing (scRNA-seq) revealed that human AP gastruloids contain cell types resembling the midbrain-hindbrain boundary (MHB), regionalized hindbrain structures (i .e. rhombomeres 1-8), regionalized neural crest (i.e. cranial, vagal, trunk)7,8 and head mesoderm. Transcriptomic comparisons to primate embryos revealed that human AP gastruloids most closely resemble Carnegie stage 11 (CS11) embryos. While they lack a notochord and full dorsal-ventral polarity, human AP gastruloids recapitulate key spatial and temporal features of early neurulation and somitogenesis. Perturbation of folic acid metabolism or rho-associated kinase (ROCK) signaling induced spinal cord defects, phenocopying aspects of spina bifida and other neural tube defects, highlighting this model's potential for studying congenital disorders9. AP gastruloids may serve as a simple, robust, scalable platform for modeling coordinated human AP body axis development. More broadly, our results suggest that controlled interactions between differentially prepatterned progenitors can initiate self-organization of complex body axis features. The "pattern-and-mix" strategy may serve as a generalizable framework for assembling spatially organized stem cell models of mammalian development.

Journal Article↗

PubMed2003

Functional divergence of two zebrafish midkine growth factors following fish-specific gene duplication.

In mammals, the unique midkine (mdk) gene encodes a secreted heparin-binding growth factor with neurotrophic activity. Here, we show the presence of two functional mdk genes named mdka and mdkb in zebrafish and rainbow trout. Both midkine proteins are clearly different from the related pleiotrophin, which was also identified in zebrafish and other fishes. Zebrafish mdka and mdkb genes map to linkage groups LG7 and LG25, respectively, both presenting synteny to human chromosome 11, in which the unique human ortholog mdk is located. At least four other genes unique in mammals are also present as duplicates on LG7 and LG25. Phylogenetic and divergence analyses suggested that LG7/LG25 paralogs including mdka and mdkb have been formed at approximately the same time, early during the evolution of the fish lineage. Hence, zebrafish and rainbow trout mdka and mdkb might have been generated by an ancient block duplication, and might be remnants of the proposed fish-specific whole-genome duplication. In contrast to the ubiquitous expression of their mammalian counterpart, zebrafish mdka and mdkb are expressed in spatially restricted, mostly nonoverlapping patterns during embryonic development and strongly in distinct domains in the adult brain. Ectopic ubiquitous expression of both mdk genes in early zebrafish embryos caused completely distinct effects on neural crest and floorplate development. These data indicate that mdka and mdkb underwent functional divergence after duplication. This provides an outstanding model to analyze the molecular mechanisms that lead to differences in pathways regulating the formation of homologous embryonic structures in different vertebrates.

Amino Acid Sequence↗

PubMed2004

T-box genes and congenital heart/limb malformations.

Congenital malformations cause significant morbidity and mortality; however, the underlying basis for many of these developmental defects is not well understood. Over the past years, a new family of genes called T-box genes has been identified that play essential roles during the development of various tissues and organs. A number of developmental syndromes have recently been shown to be linked to mutations in T-box genes, and brought direct medical relevance to their study. This review emphasizes emerging data on the molecular, cell, and disease levels, which establish a basis for parallel events in limb and heart development, and suggests that common regulatory pathways are crucial for proper differentiation and growth of these embryonic structures.

Amino Acid Sequence↗

PubMed1993

Appearance and distribution of entactin in the early chick embryo.

Entactin is a sulfated glycoprotein of basement membranes and recent data indicate that it may play a major role in extracellular matrix (ECM) assembly and in modulating the activities of the other molecular components. We investigated the time of appearance and subsequent distribution of entactin during the earliest stages of morphogenesis and its involvement in the first major cellular migrations and interactions in the chick embryo. Entactin is first detected in the epiblast and in the hypoblast at the blastula stage. The accumulating ECM displays intense presence of entactin in the space between the epiblast and the hypoblast at late blastula. Entactin is increasingly abundant in the neural plate and in the ECM and also at least transiently in many mesodermal tissues such as the notochord, the developing heart and somites in the early chick embryo. Immunogold labeling revealed a punctate pattern of entactin distribution in the ECM during the gastrula, neurula and at later stages and at all levels within the embryo. Because of its early appearance in more than one germ layer, entactin may be important in the formation of most embryonic structures. Entactin is detected at the same developmental time and co-localizes with laminin. Antibodies to entactin do not interfere with triggering of the first major cell movements but perturb directional migration of these cells. It would seem that entactin plays a functional role in the directed migration of cells and does not seem to affect cell adhesion during the period of the first morphogenetic events in the early chick embryo.

Animals↗

PubMed1991

An embryo-specific protein of barley (Hordeum vulgare).

An immunological approach has been used to identify embryo-specific products that can be used as molecular markers of embryogenesis. Immunoadsorption of antisera to remove antigens common to embryos, meristematic cells and callus, revealed one major embryo-specific antigen, a polypeptide of 17 kDa. The antigen appeared at mid-stages of zygotic embryo formation and remained at similar levels up to six days post-germination of the seedling. The polypeptide could not be detected by protein staining, suggesting it is a non-abundant product. Appearance of the antigen could be induced by culture of zygotic embryos in vitro on abscisic acid (1 microM) or mannitol (9% mass/vol.). Cross-reactive products of near-identical molecular mass were observed in embryos of wheat, rye and oats but not distantly related cereals, nor embryos from dicotyledonous species. The timing of the appearance of the antigen was different in embryos formed from microspores during anther culture in vitro. In the cultured material, the 17-kDa polypeptide preceded the appearance of morphologically distinct embryonic structure.

Abscisic Acid↗

PubMed1991

Concentrations of nuclear progesterone receptors in endometrium of virgin and repeat breeder heifers after embryo transfer.

The present study aimed to correlate the repeat breeder syndrome in the bovine with an impaired or suboptimal uterine progestational response. Concentrations of nuclear (i.e. transformed) receptors for progesterone (PRn) were determined with a binding and exchange method in endometrial samples from virgin (VH) and repeat breeder (RBH) heifers 15 days post oestrus. The heifers were recipients of Day 7 demi-embryos collected from donors with normal fertility and transferred 8 days prior to tissue sampling. Results were compared with both the type of heifer, the condition of the embryo present within the uterus and the temporal relationship to the hormone plasma levels. The binding data for PRn indicated that a single class of high-affinity, low-capacity sites existed. The amount of PRn in VH endometria holding embryonic structures was significantly greater than in RBH, but no statistical differences were found in their plasma progesterone levels. PRn concentrations were also higher in the uterine horn in which an elongated (greater than 15 mm), morphologically normal embryo was present, when compared to cornua with small (less than 5 mm) embryos, regardless of recipient group. Furthermore, in endometria with an elongated embryo in the lumen, the relative amount of PRn was significantly greater in VH than in RBH. The present results indicate that the RBH recipients of Day 7 demi-embryos by Day 15 have fewer numbers of specific receptors for maternal progesterone, which could explain in part the poorer development of the transferred embryos compared with that in virgin heifers.

Animals↗

PubMed2006

Pulmonary blastoma within bronchioloalveolar cell carcinoma.

Pulmonary blastoma is a rare tumour of the lung composed of epithelial and mesenchymal elements that morphologically resemble the embryonal structure of the lung. The authors report a 79-year-old man who was diagnosed with a pulmonary blastoma within bronchioloalveolar cell carcinoma. Macroscopic, histopathological and immunohistochemical findings suggested that the pulmonary blastoma was closely associated with the bronchioloalveolar cell carcinoma.

Adenocarcinoma, Bronchiolo-Alveolar↗

PubMed1985

Distribution of 64Cu in foetal and adult tissues in mice: influence of sodium diethyldithiocarbamate treatment.

64Cu (as 64CuCl2) was given intravenously to male C57BL mice and to pregnant C57BL mice at various stages of gestation. The disposition of the 64Cu in the adult animals and in the foetuses was studied by autoradiography and gamma spectrometry. The effects of treatments with diethyldithiocarbamate (DEDTC) on the disposition of the 64Cu in the animals were also examined. In addition, the ability of Cu to affect chondrogenesis was studied in an embryonic limb bud culture system. The results showed a strong uptake of 64Cu in the liver of the adult animals at all intervals (5 min.-24 hrs). At short survival intervals, there was also an uptake in the kidney cortex, the gastrointestinal mucosa, the adrenal, the pancreas, and the erythrocytes. Exposure to Cu may cause liver and kidney injuries, which may be related to the strong accumulation in these organs. 64Cu passed the placenta to the foetuses at all stages of gestation, although this occurred at a relatively slow rate. Within the foetuses the highest concentrations were found in the liver. Cu was observed to be toxic in the chick limb bud mesenchymal spot culture system although at relatively high concentrations. Foetal malformations and embryotoxicity may therefore be interpreted as a result of direct action of Cu on embryonic structures, although placental and/or maternal influence cannot be excluded. Pre- or posttreatment of the animals with DEDTC, which is a chelating agent, caused a very marked increase in the concentration of 64Cu in most tissues of the adult animals and also an increased foetal uptake of the metal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2004

The aryl hydrocarbon receptor is required for developmental closure of the ductus venosus in the neonatal mouse.

A developmental role for the Ahr locus has been indicated by the observation that mice harboring a null allele display a portocaval vascular shunt throughout life. To define the ontogeny and determine the identity of this shunt, we developed a visualization approach in which three-dimensional (3D) images of the developing liver vasculature are generated from serial sections. Applying this 3D visualization approach at multiple developmental times allowed us to demonstrate that the portocaval shunt observed in Ahr-null mice is the remnant of an embryonic structure and is not acquired after birth. We observed that the shunt is found in late-stage wild-type embryos but closes during the first 48 h of postnatal life. In contrast, the same structure fails to close in Ahr-null mice and remains open throughout adulthood. The ontogeny of this shunt, along with its 3D position, allowed us to conclude that this shunt is a patent developmental structure known as the ductus venosus (DV). Upon searching for a physiological cause of the patent DV, we observed that during the first 48 h, most major hepatic veins, such as the portal and umbilical veins, normally decrease in diameter but do not change in Ahr-null mice. This observation suggests that failure of the DV to close may be the consequence of increased blood pressure or a failure in vasoconstriction in the developing liver.

Animals↗

PubMed2002

Specification of jaw subdivisions by Dlx genes.

The success of vertebrates was due in part to the acquisition and modification of jaws. Jaws are principally derived from the branchial arches, embryonic structures that exhibit proximodistal polarity. To investigate the mechanisms that specify the identity of skeletal elements within the arches, we examined mice lacking expression of Dlx5 and Dlx6, linked homeobox genes expressed distally but not proximally within the arches. Dlx5/6-/- mutants exhibit a homeotic transformation of lower jaws to upper jaws. We suggest that nested Dlx expression in the arches patterns their proximodistal axes. Evolutionary acquisition and subsequent refinement of jaws may have been dependent on modification of Dlx expression.

Animals↗

PubMed1998

Developmental regulation of bicoid mRNA stability is mediated by the first 43 nucleotides of the 3' untranslated region.

During the transition from the maternal to the zygotic developmental program, the expression of genes important for pattern formation or cell cycle regulation changes dramatically. Rapid changes in gene expression are achieved in part through the control of mRNA stability. This report focuses on bicoid, a gene essential for formation of anterior embryonic structures in Drosophila melanogaster. bicoid mRNA is synthesized exclusively during oogenesis. Here, we show that bicoid mRNA stability is regulated. While bicoid mRNA is stable in retained oocytes, in unfertilized eggs, and during the first 2 h of embryogenesis, specific degradation is activated at cellularization of the blastoderm. To identify cis-acting sequences required for bicoid mRNA's regulated stability, fusions between bicoid and genes producing stable mRNAs were introduced into the Drosophila germ line by P-element-mediated transformation. The analysis of the fusion mRNAs identified a bicoid instability element (BIE) contained within a 43-nucleotide sequence immediately following the stop codon. The BIE is sufficient to destabilize the otherwise-stable ribosomal protein A1 mRNA and is separable from the previously identified bicoid mRNA localization signals and from the "nanos response element." Similar mechanisms may regulate a class of developmentally important maternal genes whose mRNA has a temporal profile similar to that of bicoid.

Animals↗

PubMed2000

Expression and functional analysis of Uch-L3 during mouse development.

Mice homozygous for the s(1Acrg) deletion at the Ednrb locus arrest at embryonic day 8.5. To determine the molecular basis of this defect, we initiated positional cloning of the s(1Acrg) minimal region. The mouse Uch-L3 (ubiquitin C-terminal hydrolase L3) gene was mapped within the s(1Acrg) minimal region. Because Uch-L3 transcripts were present in embryonic structures relevant to the s(1Acrg) phenotype, we created a targeted mutation in Uch-L3 to address its role during development and its possible contribution to the s(1Acrg) phenotype. Mice homozygous for the mutation Uch-L3(Delta3-7) were viable, with no obvious developmental or histological abnormalities. Although high levels of Uch-L3 RNA were detected in testes and thymus, Uch-L3(Delta3-7) homozygotes were fertile, and no defect in intrathymic T-cell differentiation was detected. We conclude that the s(1Acrg) phenotype is either complex and multigenic or due to the loss of another gene within the region. We propose that Uch-L3 may be functionally redundant with its homologue Uch-L1.

Amino Acid Sequence↗