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PubMed2006

Epigenetics of lung cancer.

Epigenetics is the study of heritable changes in gene expression that occur without changes in DNA sequence. It has a role in determining when and where a gene is expressed during development. Perhaps the most well known epigenetic mechanism is DNA methylation whereby cytosines at position 5 in CpG dinucleotides are methylated. Histone modification is another form of epigenetic control, which is quite complex and diverse. Histones and DNA make up the nucleosome which is the structural unit of chromatin which are involved in packaging DNA. Apart from the crucial role epigenetics plays in embryonic development, transcription, chromatin structure, X chromosome inactivation and genomic imprinting, its role in an increasing number of human diseases is more and more recognized. These diseases include cancer, and lung cancer in particular has been increasingly studied for the potential biological role of epigenetic changes with the promise of better and novel diagnostic and therapeutic tools.

DNA Methylation↗
PubMed1986

Cell surface glycoconjugates and carbohydrate-binding proteins: possible recognition signals in sensory neurone development.

Dorsal root ganglion (DRG) neurones transmit cutaneous sensory information from the periphery to the dorsal horn of the spinal cord. Subpopulations of DRG neurones that subserve distinct sensory modalities project to discrete regions in the dorsal horn. The formation of specific sensory connections during development may involve cell-surface interactions with spinal cord cells. Molecules that are expressed on the surface of functional subpopulations of DRG and dorsal horn neurones have therefore been identified. Distinct subsets of DRG neurones express globo- or lactoseries carbohydrate differentiation antigens. The expression of defined carbohydrate structures correlates with the embryonic lineage, peptide phenotype and the central termination site of DRG neurones. Similar or identical glycoconjugates have been implicated in cellular interactions that contribute to preimplantation embryonic development. Small-diameter DRG neurones that project to the superficial dorsal horn express N-acetyllactosamine backbone structures that are potential ligands for beta-galactoside-specific binding proteins (lectins). Two lectins have been identified that are expressed early in development in the superficial dorsal horn. These complementary molecules may contribute to the development of sensory afferent projections in the spinal cord.

Aging↗
PubMed1983

Investigations on myelination in vitro: IV. "Myelin-like" or premyelin structures in cultures of dissociated brain cells from 14--15-day-old embryonic mice.

The present study reports ultrastructural and biochemical data characteristic of myelin-related structures in 30- to 41-day-old cultures of dissociated brain cells from 14- to 15-day-old embryonic mice. Multilayered membranous material was identified and displayed an alternation of electron-lucent and electron-dense lamellae with a periodicity of 102 A. In these membranes, typical myelin constituents like basic protein, cerebrosides, sulfatides, and CNPase could be identified. Although we are still unable to distinguish if these membranes are premyelin or compact myelin, which could be partly degraded, these results indicate that cultured mouse brain cells retain, to a certain extent, potential to produce myelin-related membranes.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed2005

Beta-catenin-mediated cell-adhesion is vital for embryonic forebrain development.

Forming a complex structure such as the mammalian brain requires a complex interplay between cells and different signalling cascades during embryonic development. beta-catenin plays pivotal roles in these processes by mediating cadherin-based cell adhesion and Wnt signalling. We show for the first time that beta-catenin functions predominantly as a mediator of cell adhesion during early development of the mammalian telencephalon. Immunohistochemical analysis demonstrates that beta-catenin is localized, together with N-cadherin, to adhesion junctions at the apical lining of the neuroepithelium. The ablation of beta-catenin specifically from the forebrain leads to a disruption of apical adherens junctions and a breakdown of neuroepithelial structures. We show that beta-catenin-deficient neuroepithelial cells delaminate and undergo apoptosis. Newborn beta-catenin mutants lack the entire forebrain and anterior facial structures. Our data also indicate a lack of TCF/LEF-beta-catenin-dependent transcriptional activity in the telencephalon of Wnt reporter embryos. Together with the absence of nuclear beta-catenin, this finding suggests that canonical Wnt signalling is not active during early telencephalic development. In summary, we demonstrate that beta-catenin mediates cell-cell adhesion in the early telencephalon and is vital for maintaining the structural integrity of the neuroepithelium.

Adherens Junctions↗
PubMed2001

TGFbeta2 in embryos with inborn anomalies: effect of maternal immunopotentiation.

PROBLEM: TGFbetas are among the main immunoregulatory molecules contributing to successful embryonic development. Besides, our and other studies revealed that maternal immunopotentiation has a potential to increase the resistance of the embryo to the teratogenic insult. This work was designed to evaluate: (1) whether the formation of teratogen-induced anomalies is accompanied by an altered pattern of TGFbeta2 expression in embryonic cells and (2) whether maternal immunopotentiation modifies the pattern of TGFbeta2 expression in embryos responding to the teratogenic insult. METHOD OF STUDY: Experiments were performed in embryos of ICR mice exposed to 15 and 40 mg/kg of a reference teratogen, cyclophosphamide (CP) on day 12 of gestation. A group of mice was immunopotentiated with xenogeneic rat splenocytes 21 hr before the beginning of mating. Embryos were examined for the occurrence of gross structural anomalies 24 and 72 hr after CP treatment. Then, immunohistohemistry and in situ hybrydization assays were used to evaluate the expression of TGFbeta2 protein and mRNA in the brain, face, limbs and liver of these embryos. RESULTS: No external anomalies were observed in embryos examined 24 hr after CP treatment. Embryos examined 72 hr after CP treatment at 40 mg/kg exhibited agnathia, micrognathia, kinky tail, phocomelia, but no signs of dismorphogenesis were observed in the liver at the organ level. A significant increase in the expression of TGFbeta2 mRNA was observed in cells, residing in the brain, face and limbs but not in the liver of CP-exposed embryos tested 24 hr after CP injection in both doses. The level of TGFbeta2 protein in these embryos did not differ from that of controls. In embryos tested 72 hr after CP injection in the high dose both TGFbeta2 protein and mRNA expression were found to be elevated. Maternal immunopotentiation while enhancing the embryo's resistance to CP practically abolished an elevated expression of the TGFbeta2 mRNA detected in tested organ structures of embryos of non-immunopotentiated CP treated mice 24 hr after CP injection in both the low and the high doses. Also, a significant decrease in the level of TGFbeta2 mRNA expression was observed in embryos of immunopotentiated mice examined 72 hr after CP treatment. CONCLUSIONS: The results of this work show a possible involvement of TGFbeta2 in the formation of teratogen-induced structural anomalies and suggest that the stimulation of the maternal immune system may realize its protective effect by normalizing the level of TGFbeta2 expression in teratogen-targeted embryonic structures.

Abnormalities, Drug-Induced↗
PubMed2004

Embryonic development of the ganglion plexuses and the concentric layer structure of human gut: a topographical study.

In this study, we performed a detailed topographical study on the development of ganglion plexuses and the smooth muscle layers of human embryonic and fetal gut. Neuron and glia differentiation was investigated with anti-PGP9.5 and anti-S100 antibodies respectively. The differentiation of smooth muscle and interstitial cells of Cajal (ICC) was studied with anti-smooth muscle alpha-actin and anti-C-Kit antibodies respectively. By week 7, rostro-caudal neural crest cell (NCC) colonization of the gut was complete, and NCCs have differentiated into neurons and glia. At the foregut, neurons and glia were aggregated into ganglion plexus in the myenteric region, and the longitudinal and circular muscle layers have started to differentiate; however, neurons and glia were not found in the submucosa. At the hindgut, neurons and glia were dispersed within the mesenchyme. Myenteric plexus, longitudinal and circular muscle layers formed along the entire gut by week 9. Scattered and individual neurons and glia, and small ganglion plexuses were detected in the foregut and midgut submucosa by week 12. Ganglion plexus was not seen in the hindgut submucosa until week 14. Muscularis mucosae was formed at the foregut and midgut by week 12 but was only discernible at the hindgut 2 weeks later. As the gut wall developed, ganglion plexus increased in size with more neurons and glia, and the formation of intra-plexus nerve fascicle. ICCs were localized in the ganglion plexus as early as week 7. ICCs were initially dispersed in the plexus and were preferentially localized at the periphery of the plexus by week 20. The specification of the annular layers of human embryonic and fetal gut follows a strict spatio-temporal pattern in a rostro-caudal and centripetal manner suggesting that interaction between (1) homotypic and/or heterotypic cells; and (2) cells and the extracellular matrix is critical for the embryonic development of the gut mesenchyme and the enteric nervous system.

Actins↗
PubMed2004

Bsx, an evolutionary conserved Brain Specific homeoboX gene expressed in the septum, epiphysis, mammillary bodies and arcuate nucleus.

Shaping and orchestrating the genetic program involved in embryonic modelling of brain structures is a major function played by homeobox containing genes. Recently, analysis of conditional mouse mutants has pointed out additional roles in supporting adult brain functional activities. During a search for novel homeobox genes in the public released genomic sequences derived by the Human and Mouse genome projects, we were able to identify the mouse homologue of the Drosophila brain specific homeobox gene. We named it Bsx and characterized its expression in embryonic and post-natal mouse brain. Interestingly, Bsx shows an expression pattern restricted to a few specific developing brain structures. Pineal gland, telencephalic septum, hypothalamic pre-mammillary body and arcuate nucleus are the only brain structures where we detected Bsx transcriptional activity, which is maintained also after birth. In particular, Bsx might be considered an important molecular marker for early embryonic stages of epiphysis development, being specifically expressed in this neural structure from E9.5 onwards.

Amino Acid Sequence↗
PubMed1984

Neural crest and normal development: a new perspective.

Several clinical syndromes, including the DiGeorge syndrome, are characterized by clusters of developmental defects of the heart and great vessels with structures derived from the embryonic pharyngeal apparatus including thymus and parathyroids. The connective tissue derivatives of neural crest are necessary for the normal development of these structures, and there is new experimental evidence that depletion of neural crest causes defects similar to these clinical syndromes. Therefore it is proposed that many of these syndromes are due to inappropriate development of neural crest. The implications of this hypothesis include the predictions 1) that asplenia and certain other anomalies have the same etiology, and 2) that it is possible to observe the effects of teratogenic agents upon a cellular population (neural crest) at the time when it is being altered, rather than waiting until definitive organs may be examined.

Abnormalities, Multiple↗
PubMed1994

Ethyl alcohol reduces cardiac output, stroke volume, and end diastolic volume in the embryonic chick.

It has been established that ethanol causes both human congenital cardiac malformations and structural intracardiac abnormalities in the embryonic chick. In view of a theory that reduced embryonic tissue hemodynamics are associated with the development of malformations, we attempted to determine whether or not a) ethanol altered cardiac blood flow and b) altered hemodynamics were a function of ethanol dose in the chick embryo. Cardiac function in Hamburger-Hamilton stage 19 chick embryos was recorded on videotape before and up to 10 hours after exposure to graded doses of ethanol. Parameters of cardiac function, including cardiac output, were determined from videotaped images by means of computer assistance. Cardiac output decreased in a linear fashion with dose for up to 3 hours after exposure to ethanol. The maximum relative percent decrease in cardiac output was directly related to the dose of ethanol administered. Furthermore, the time required after ethanol treatment for mean cardiac output to return to pretreatment and control values was also dose-dependent--lower doses of ethanol required less time for mean cardiac output to return to pretreatment and control values. Although relatively high doses of ethanol depress cardiac rate, we attribute the significant decrease in cardiac output primarily to parallel dose-dependent decreases in both stroke volume and end diastolic volume. Our data are consistent with the hypothesis that reduced embryonic cardiac blood flow during cardiogenesis is associated with the development of ethanol-induced intracardiac defects in chick embryos.

Animals↗
PubMed2002

NF-kappa B DNA-binding activity in embryos responding to a teratogen, cyclophosphamide.

BACKGROUND: The Rel/NF-kappaB transcription factors have been shown to regulate apoptosis in different cell types, acting as inducers or blockers in a stimuli- and cell type-dependent fashion. One of the Rel/NF-kappaB subunits, RelA, has been shown to be crucial for normal embryonic development, in which it functions in the embryonic liver as a protector against TNFalpha-induced physiological apoptosis. This study assesses whether NF-kappaB may be involved in the embryo's response to teratogens. Fot this, we evaluated how NF-KappaB DNA binding activity in embryonic organs demonstrating differential sensitivity to a reference teratogen, cyclophosphamide, correlates with dysmorphic events induced by the teratogen at the cellular level (excessive apoptosis) and at the organ level (structural anomalies). RESULTS: The embryonic brain and liver were used as target organs. We observed that the Cyclophosphamide-induced excessive apoptosis in the brain, followed by the formation of severe craniofacial structural anomalies, was accompanied by suppression of NF-kappaB DNA-binding activity as well as by a significant and lasting increase in the activity of caspases 3 and 8. However, in the liver, in which cyclophosphamide induced transient apoptosis was not followed by dysmorphogenesis, no suppression of NF-kappaB DNA-binding activity was registered and the level of active caspases 3 and 8 was significantly lower than in the brain. It has also been observed that both the brain and liver became much more sensitive to the CP-induced teratogenic insult if the embryos were exposed to a combined treatment with the teratogen and sodium salicylate that suppressed NF-kappaB DNA-binding activity in these organs. CONCLUSION: The results of this study demonstrate that suppression of NF-kappaB DNA-binding activity in embryos responding to the teratogenic insult may be associated with their decreased resistance to this insult. They also suggest that teratogens may suppress NF-kappaB DNA-binding activity in the embryonic tissues in an organ type- and dose-dependent fashion.

Abnormalities, Multiple↗
PubMed2026

Developmental origins of pregnancy loss in cattle.

Pregnancy losses constitute a major economic burden in cattle farming and are caused by developmental failures occurring mostly during the first month of gestation. This review integrates knowledge gathered from direct and indirect estimations of embryo survival at critical developmental periods with knowledge obtained from functional in vivo and in vitro studies to elucidate the developmental origins of pregnancy loss in cattle. Fertilization failures and embryonic arrest prior to the blastocyst stage, estimated based on morphological observation of flushed structures, average 10 to 20 and 10 to 30%, respectively. Reduced oocyte competence arises as the major driver of the underlying developmental failures, including impaired embryonic genome activation, loss of totipotency and defective first lineage differentiation. To estimate embryonic losses from blastocyst to implantation, direct observation of embryo development and indirect proxies of pregnancy have been employed. Indirect proxies such as nonreturn to oestrus or biochemical markers such as Interferon Stimulated Genes or Pregnancy Associated Glycoproteins inform on the development of extra-embryonic membranes, but do not distinguish between viable pregnancies and anembryonic pregnancies, where embryo-devoid structures formed by extra-embryonic membranes are able to maintain the corpus luteus to day 37. Merging data from recovery rates of early elongated structures and incidence of embryo-devoid structures, embryonic mortality from blastocyst hatching to pregnancy recognition oscillates between 12-79% for in vivo derived and 40-86% for in vitro produced embryos. The exclusion of anembryonic pregnancies diminishes embryonic mortality between day 16 and the time when the embryo proper is clearly identifiable by ultrasound (days 31-42) to less than 10%. The manuscript also provides an update on novel tools used to elucidate embryonic metabolic and signalling requirements, as well as on the molecular regulation of key developmental landmarks that must be achieved during developmental windows most susceptible to pregnancy loss.

cattle↗
PubMed1986

Transient midline raphe glial structure in the developing rat.

A major glial structure is present during development within the midline raphe of the midbrain, hindbrain, and cervical spinal cord of the rat. It is composed of great numbers of glial cell bodies lying immediately ventral to the cerebral ventricular system and the large radial processes extending from these cells toward the ventral surface of the brain roughly within the midsagittal plane. There is also a smaller group of glial cells on the dorsal surface of the aqueduct and the central canal whose processes extend to the dorsal surface of the brain. The entire structure exhibits an intensely positive immunoreactivity with the antibody to the S-100 protein, a nervous-system-specific protein found primarily in the cytoplasm of astrocytes. This immunoreactivity makes possible a clear visualization of the extent, magnitude, and continuity of this structure from at least embryonic day 15, the first age examined, until postnatal days 7-8, when it is no longer visible by this technique. This glial structure has several prominent morphological characteristics. During prenatal and early postnatal development the fibers forming the ventral aspect of the structure in the midbrain and hindbrain are formed into two parallel plates on either side of the midline with S-100-negative tissue between the plates. As development progresses, S-100-positive fibers are continually added so that the plates become thicker at the expense of the nonstaining intervening area. By postnatal day 4 only a single midline plate of fibers is visible, occupying the entire midline raphe. In the region of the pontine flexure the entire structure takes on a distinctly pleated configuration. This fact produces a curious "sine wave" appearance when the plane of section crosses these vertical pleats. At postnatal day 5 the structure begins to disappear, and it is no longer visible by 7-8 days postnatal. This glial structure does not stain with antisera to glial fibrillary acidic protein, a protein associated with fibrous astrocytes, or routine cell stains such as cresyl violet. With these techniques the raphe area appears essentially devoid of identifiable cellular elements.

Animals↗
PubMed1995

Isolation and structural determination of seminal vesicle-specific peptides of the terrestrial isopod, Armadillidium vulgare.

During the course of purifying the androgenic gland hormone of the terrestrial isopod, Armadillidium vulgare, that induces post-embryonic sex differentiation, four structurally related peptides were obtained and their structures determined by a combination of microsequence and mass spectral analyses. These peptides were found to exist speciffically in the seminal vesicle and vas deferens by a Western blot analysis, therefore being designated as seminal vesicle-specific peptides (SVSPs). They had essentially the same amino acid sequences but differed from one another in the truncation of several residues at the N-terminus and of one residue at the C-terminus, and in the modification of glutamine to pyroglutamate at the N-terminus. The longest peptides, SVSP-4, consisted of 60 amino acid residues with two intramolecular disulfide bridges. There is no significant homology with any other vertebrate or invertebrate peptides.

Amino Acid Sequence↗
PubMed1992

Use of embryonic stem cells to study mutations affecting postimplantation development in the mouse.

The generation and analysis of insertional mutations that perturb early postimplantation development provide a means to identify genes required at this stage of embryogenesis. We have been studying two independently generated insertional mutations termed 413.d and H beta 58 that result in early postimplantation lethality. Each mutation is associated with a distinct phenotype. 413.d mutant embryos become profoundly abnormal around the time of gastrulation: no identifiable embryonic axis or mesodermal structures are formed. H beta 58 mutant embryos proceed further in development, forming a relatively normal anteroposterior axis before developmental arrest occurs. We isolated embryonic stem cell lines homozygous for each of these mutations and assessed their differentiation abilities and developmental potential in vitro and after their introduction into wild-type blastocysts. From these studies we conclude that the 413.d mutation acts in a non-cell-autonomous fashion: mutant cells appear capable of participating, in conjunction with wild-type cells, in the formation of derivatives of all three primary cell lineages of the embryo. H beta 58 mutant embryonic stem cells are clearly pluripotent but they appear to be more restricted in their developmental potential, suggesting that the H beta 58 gene product may be required by specific tissues of the embryo.

Animals↗
PubMedDate not supplied

Maternal expression and early zygotic regulation of the Hox3/zen gene in the grasshopper Schistocerca gregaria.

In insects, a key step in the early patterning of the egg is to distinguish the primordium of the embryo proper from those regions that will form extra-embryonic membranes. In Drosophila, where these processes are well understood, the structure of the extra-embryonic membranes is highly derived. The distinct amnion and serosa typical of lower insects is replaced by a single, fused, and much reduced membrane, the amnioserosa, which never secretes an embryonic cuticle. We have used the Zen gene as a marker to study the formation of the extra-embryonic membranes, and other aspects of early embryonic patterning, in the grasshopper Schistocerca gregaria (African Plague Locust). Zen genes are derived from Hox genes, but in Drosophila they appear to have lost any role in patterning the A/P axis of the embryo; instead, they are involved in D/V patterning and the specification of the extra-embryonic membranes. We show that the Schistocerca zen gene is expressed during embryogenesis in three distinct phases. The first of these is during cleavage, when Sgzen is transiently expressed in all energids that reach the cell surface. The second phase of expression initiates in a ring of "necklace cells" that surround the forming embryo, and demarcate the boundary between the amnion and serosa. This leads to expression throughout the serosa. The final phase of expression is in the amnion, after this has separated from the serosa. This complex pattern implies that the role of Sgzen in Schistocerca is not limited solely to the specification of cell identity in the extra-embryonic membranes. We also report that the Schistocerca zen gene is expressed maternally, unlike its Drosophila and Tribolium counterparts. A distinct maternal transcript, and maternal Zen protein, accumulate in the developing oocyte from early post-meiotic stages. They remain uniformly distributed in the oocyte cytoplasm until late vitellogenic stages, when the protein and RNA become somewhat concentrated at the egg cortex and in the posterior polar cap of the oocyte, probably by passive exclusion from the yolk. The cytoplasmic localization of Sgzen protein in the oocyte, and at some stages during embryogenesis, implies that nuclear exclusion of this transcription factor is specifically controlled.

Animals↗
PubMed1991

Neurotrophins: structural relatedness and receptor interactions.

Nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) are structurally related proteins that allow the survival of specific populations of embryonic vertebrate neurons. The primary structure of these neurotrophins, deduced from their nucleotide sequences, indicates that all three are synthesized in the form of precursor proteins presumably allowing for appropriate folding, including the formation of disulphide bridges, cleavage and secretion. While no information is yet available on the 3-dimensional structures of the neurotrophins, results from binding studies using the three neurotrophins as ligands indicate that their receptors do recognize similarities, as well as differences, between them. High-affinity receptors, that presumably mediate the biological response, as well as low-affinity receptors are present on neurons responsive to the neurotrophins. Whereas a large excess of heterologous ligand is needed to reduce binding of a particular neurotrophin to its high-affinity receptor, the same concentration of homologous or heterologous ligand similarly reduce the binding of any of the three neurotrophins to the low-affinity receptor. For all three, the low-affinity receptor appears to be the already characterized NGF low-affinity receptor that seems to be an integral part of the high-affinity receptor complexes. These results suggest that the regulation of neuronal survival by target cells can, in part, be explained by the release from these cells of limiting quantities of the structurally related neurotrophins, each being recognized by a specific high-affinity receptor complex located on the nerve terminals of the responsive neurons.

Animals↗
PubMed1992

The biological activity of hydrogen peroxide. V. The crystal structure of a histidine-peroxide adduct and its biological activities.

Crystals were prepared from a mixture of L-histidine (L-His) and hydrogen peroxide (H2O2) and tested for biological activity in human embryonic fibroblasts. The crystal structure was determined by X-ray diffraction to be that of an adduct, in which the H2O2 molecule forms a OH-N hydrogen bond with N delta of the side chain of L-His. A 10-min treatment with this adduct in solution (25-150 microM) induced more marked chromosomal aberrations and more single-strand breaks (SSB) in DNA than H2O2 itself, and these effects were generated in a dose-dependent manner. With respect to the induction of dicentric and ring chromosomes (Dic and Ring), a maximum frequency of 1.3 per cell was obtained at 75 microM. This maximum level of induction by the adduct was 6-7 times higher than that by H2O2 and was comparable to that by the mixture of L-His and H2O2 which we observed in our previous studies. The most effective dose for such induction by the adduct was also similar to that of L-His in the mixture. Cell growth was inhibited more strongly by the adduct than by H2O2 alone after a 60-min treatment at 75 microM, although there was not much difference between their effects after a 10-min treatment at 75 microM. The reactive factors derived from the adduct were the same as those in the mixture, and are suggested to be derivatives of H2O2, hydroxyl radicals (.OH) and/or singlet oxygen (1O2). Thus the patterns of induction and kinetics of the biological activities of the adduct were very similar to those of the mixture, but not to those of H2O2. These results suggest that the formation of the adduct plays an important role in the enhancement of the expression of the biological activity of H2O2 by the coadministration of L-His and H2O2, which we observed in our previous study.

Catalase↗