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PubMed2001

Changes in DNA loop domain structure during spermatogenesis and embryogenesis in the Syrian golden hamster.

The DNA in eukaryotic cells is organized into loop domains that are 25 to 100 kilobases long and attached at their bases to the nuclear matrix. This organization plays major roles in DNA replication and transcription. We examined changes in DNA loop structure of the 5S rDNA gene cluster in the Syrian golden hamster as a function of cellular differentiation by direct visualization with fluorescent in situ hybridization. The 5S rDNA cluster is large enough to encompass more than one loop domain but small enough that individual loop domains can still be resolved. We found that the sizes of the 5S rDNA loops are much smaller, and that the numbers of loops per locus are larger, in all pluripotent cell types than they are in adult somatic tissue. Within the pluripotent spermatogenic cell lineage, the loop domain organization was cell specific. The loop size decreased during the early stages of spermatogenesis but did not change during spermiogenesis, suggesting that DNA loop structure is independent of the chromatin condensation that occurs when protamines replace histones. In early embryonic cells, the loop structure remained small, but in differentiated somatic cells, it became much larger. We suggest that these changes in the 5S rDNA loop domain structure may be related to the maintenance or loss of developmental potential.

Animals↗
PubMed1988

Ontogeny of structural components at the dermal-epidermal junction in human embryonic and fetal skin: the appearance of anchoring fibrils and type VII collagen.

The ontogeny and composition of the dermal-epidermal junction (DEJ) in developing human embryonic and fetal skin was studied at progressive stages of gestation by immunofluorescence microscopy and immunocytochemistry using transmission electron microscopy (TEM). The DEJ of embryonic skin at 5 weeks estimated gestational age (EGA) was a simple basement membrane zone limited to the basal cell plasma membrane, lamina lucida, and lamina densa. A network of reticular collagen fibrils (reticular lamina) was deposited beneath the lamina densa by 6 weeks. Coincident with the onset of increased complexity in epidermal and dermal structure, at the time of the embryonic to fetal transition, the DEJ displayed additional components that were markers of maturation. At 7-8 weeks EGA, fine filamentous structures extended from the DEJ into the reticular lamina. By 9 weeks EGA hemidesmosomes and banded anchoring fibrils were recognizable, although distributed sparsely at the DEJ. With increasing gestational age, these structures displayed greater electron density and structural completeness. By the end of the first trimester, the DEJ appeared ultrastructurally similar to that of mature skin. Weak immunofluorescent labeling demonstrated the presence of type VII collagen at the DEJ by 8 weeks EGA. From 10-12 weeks EGA immunofluorescent labeling of the DEJ for type VII collagen was distinctly punctate, while immunoperoxidase labeling observed by TEM was linear, continuous, and sublamina densa in position. With ongoing gestation the immunofluorescent labeling became increasingly stronger at the DEJ. Thus, type VII collagen was present at the DEJ in the zone immediately beneath the lamina densa, before the appearance of mature anchoring fibrils but coordinate with the appearance of fine filamentous, unbanded structures, and appeared to increase with the development and accumulation of anchoring fibrils.

Collagen↗
PubMed2006

Therapeutic potential of stem cells in diabetes.

Stem cells possess the ability to self-renew by symmetric divisions and, under certain circumstances, differentiate to a committed lineage by asymmetric cell divisions. Depending on the origin, stem cells are classified as either embryonic or adult. Embryonic stem cells are obtained from the inner cell mass of the blastocyst, a structure that appears during embryonic development at day 6 in humans and day 3.5 in mice. Adult stem cells are present within tissues of adult organisms and are responsible for cell turnover or repopulation of tissues under normal or exceptional circumstances. Taken together, stem cells might represent a potential source of tissues for cell therapy protocols, and diabetes is a candidate disease that may benefit from cell replacement protocols. The pathology of type 1 diabetes is caused by the autoimmune destruction or malfunction of pancreatic beta cells, and consequently, a lack of insulin. The absence of insulin is life-threatening, thus requiring diabetic patients to take daily hormone injections from exogenous sources; however, insulin injections do not adequately mimic beta cell function. This results in the development of diabetic complications such as neuropathy, nephropathy, retinopathy and diverse cardiovascular disorders. This chapter intends to summarize the possibilities opened by embryonic and adult stem cells in regenerative medicine for the cure of diabetes.

Animals↗
PubMed2001

The structure-specific endonuclease Ercc1-Xpf is required for targeted gene replacement in embryonic stem cells.

The Ercc1-Xpf heterodimer, a highly conserved structure-specific endonuclease, functions in multiple DNA repair pathways that are pivotal for maintaining genome stability, including nucleotide excision repair, interstrand crosslink repair and homologous recombination. Ercc1-Xpf incises double-stranded DNA at double-strand/single-strand junctions, making it an ideal enzyme for processing DNA structures that contain partially unwound strands. Here we demonstrate that although Ercc1 is dispensable for recombination between sister chromatids, it is essential for targeted gene replacement in mouse embryonic stem cells. Surprisingly, the role of Ercc1-Xpf in gene targeting is distinct from its previously identified role in removing nonhomologous termini from recombination intermediates because it was required irrespective of whether the ends of the DNA targeting constructs were heterologous or homologous to the genomic locus. Our observations have implications for the mechanism of gene targeting in mammalian cells and define a new role for Ercc1-Xpf in mammalian homologous recombination. We propose a model for the mechanism of targeted gene replacement that invokes a role for Ercc1-Xpf in making the recipient genomic locus receptive for gene replacement.

Animals↗
PubMed2003

Can we identify novel angiogenesis inhibitors from cultured embryonic cells?

The first vascular structures in embryos are formed by vasculogensis, the de novo formation of blood vessels from angioblasts. However, angiogenesis, the sprouting of capillaries from pre-existing blood vessels, are also involved in the development of embryonic vascular system in certain organs, such as the kidney or the brain. These facts led us to speculate that embryonic tissues could produce potent angiogenesis inhibitors as well to refine the primitive vascular development. In the present study, we found that two different types of cultured human embryonic cells, 293T and WI-38, produced soluble factors that completely inhibited angiogenic effects of vascular endothelial growth factor on microvascular endothelial cells. Since angiogenesis is related to various pathological states, including tumor growth and metastasis and diabetic retinopathy, to identify novel potent angiogenesis inhibitors from cultured embryonic cells by differential display techniques or DNA microarray technology might be a valuable strategy to develop a novel therapeutic approach.

Angiogenesis Inhibitors↗
PubMed1997

Characterization of monoclonal antibodies against tenascin-C: no apparent effect on kidney development in vitro.

Tenascin-C is an extracellular matrix glycoprotein found in embryonic mesenchyme. The precise biological function of tenascin-C is unknown, but different parts of the molecule have effects on cell adhesion and other cellular activities. We studied the expression and role of tenascin-C in the embryonic mouse kidney. By Northern blots, no tenascin-C was detectable in uninduced mesenchyme from day 11 embryonic kidneys, but after 24 hours of in vitro culture both major splice variants of tenascin-C were detected. The larger variant was the predominant form. By in situ hybridization tenascin-C mRNA in 13-day old embryonic kidneys was detected in the mesenchyme surrounding newly formed epithelial structures. In 17-day old embryonic kidneys, tenascin-C mRNA was detected in mesenchyme around the forming epithelial structures in the cortex, and expression was also seen in mesenchyme surrounding the capsular epithelium of glomeruli. In newborn kidneys, expression had shifted to the medulla but was still confined to mesenchymal areas. We have characterized 6 new monoclonal antibodies against mouse tenascin-C, which all stain embryonic kidneys from different stages in a pattern consistent with earlier reports and with the mRNA data. The binding sites of the monoclonal antibodies on the tenascin-C molecule were mapped to discrete regions of tenascin-C. These six and five previously described antibodies against tenascin-C were tested in antibody perturbation experiments. Three of these have been shown by in vitro assays to perturb function of other cell types. Despite this, none of them inhibited development of mouse kidneys in organ culture, although they were tested at 1 mg/ml. It raises the possibility that tenascin-C is not crucial for kidney development. Alternatively, tenascin-C has more subtle functions which could not be identified with the assays used here.

Animals↗
PubMed1995

A Xenopus laevis gene encoding EF-1 alpha S, the somatic form of elongation factor 1 alpha: sequence, structure, and identification of regulatory elements required for embryonic transcription.

Transcription of the Xenopus laevis EF-1 alpha S gene commences at the mid-blastula stage of embryonic development and then continues constitutively in all somatic tissues. The EF-1 alpha S promoter is extremely active in the early Xenopus embryo where EF-1 alpha S transcripts account for as much as 40% of all new polyadenylated transcripts. We have isolated the Xenopus EF-1 alpha S gene and used microinjection techniques to identify promoter elements responsible for embryonic transcription. These in vivo expression studies have identified an enhancer fragment, located approximately 4.4 kb upstream of the transcription start site, that is required for maximum expression from the EF-1 alpha S promoter. The enhancer fragment contains both an octamer and a G/C box sequence, but mutation studies indicate that the octamer plays no significant role in regulation of EF-1 alpha S expression in the embryo. The presence of a G/C element in the enhancer and of multiple G/C boxes in the proximal promoter region suggests that the G/C box binding protein, Sp1, plays a major role in the developmental regulation of EF-1 alpha S promoter activity.

Amino Acid Sequence↗
PubMed1984

Structural change of myofibrils during mitosis of newt embryonic myocardial cells in culture.

Newt embryonic myocardial cells can undergo mitosis in culture. The successive changes in the striation pattern of sarcomeres of myofibrils during mitosis were studied by polarization microscopy without fixing or killing the cells. Birefringence of well-organized striation patterns, i.e., bright A-bands and dark I-bands, was clearly visible in interphase cells and did not show any detectable changes during incubation for 3 h or more. Electron microscopy showed the presence of well-organized myofibrils with Z-bands in these interphase cells. When myocardial cells entered the mitotic stage, the birefringence of striation pattern of their myofibrils gradually changed with the pattern in small parts of the myofibrils gradually becoming indistinct (called 'indistinct striation' in this paper). These indistinct regions increased in size during the mitotic stage. In addition, in some regions of the indistinct striation, the birefringence of sarcomeres gradually decreased and finally disappeared (called 'disappearance of sarcomeres' in this paper). No myocardial cells underwent mitosis without these disruptive changes of the myofibril striation patterns. In the post-mitotic stage, the well-organized striation of the myofibrils reappeared. Electron microscopy showed disorganized sarcomeres without Z-bands in the regions of indistinct striation, and no well-organized myofibrils in the regions where the sarcomeres had disappeared. Thus the well-organized myofibrils with Z-bands became transiently disorganized at least in some parts, during mitosis. They were then reorganized into daughter myocardial cells.

Animals↗
PubMed1975

[Investigations on the mutagenic effect of triethylenemelamine (TEM) on early embryonic tissue and bone marrow of the rat by chromosome analysis (author's transl)].

Female rats were treated with triethylenemelamine (Tretamine; TEM) with a dose of 0.4 mg/kg body weight and 0.6 mg/kg body weight respectively on days 1, 2, 3; 3, 4, 5 or 6, 7, 8 post coitum. The animals were slaughtered on day 9 or pregnancy. Corpora lutea and living and dead embryos were counted to estimate embryonic loss. Thereafter chromosome-analysis of bone marrow cells and embryonic tissue took place. Highter TEM dosage increased the rate of embryonic loss. It increased from 28.1% with a dose of 3 X 0.4 mg TEM to 75.7% with 3 X 0.6 mg TEM. The level of embryonic loss depends on the time of treatment during different stages of early gestation. It was highest on the first 3 days and lowest on days 6-8 of gestation (0.4 mg TEM on -ays 1, 2, 3 p.c., 71.8%; 0.4 mg TEM on days 6, 7, 8 p.c., 2.9%). By the chromosome analysis, early embryonic tissue seemed to be more sensitive to TEM than bone marrow cells. The highest rates of numerical (35.7%) and (3 X 0.4 mg TEM). A higher dose induced a negative dose-effect, the frequency of aberrations decreased (3 X 0.6 mg TEM, 29% NUMERICAL AND 1.2% STRUCTURal aberrations). With increased embryonic loss (from 28.1% to 75%) structural aberrations decreased (from 5.7% to 1.2%). The time of treatment p.c. was highly correlated with the frequency of aberrations. It was highest with TEM application on days 6, 7, 8 of pregnancy; at the same time the mortality rate was lowest. The same tendencies were noted in the investigation of the chromosomes from bone marrow cells.

Animals↗
PubMed1997

A Streptomyces fradiae protease dissociates structurally preserved neurons and glial cells from the embryonic and adult central nervous system of vertebrates.

Nerve cell dissociation has become a key procedural tool in the implementation of a number of techniques in cellular and molecular neurobiology. We report that a protease preparation from Streptomyces fradiae (henceforth SF-protease) dissociates viable and morphologically identifiable embryonic and mature neurons and glial cells from the central nervous system of chick and rat, when used under strictly controlled conditions. Typical dendritic and axonal growth cones, with their lamellipodia and filopodia, are seen in many neuroblast types - growth cones in the case of embryonic glial cells and even the thinnest processes of some cells, such as the microvilli of adult chick retinal Müller (glial) cells, or the cilia of photoreceptors appear intact. Our results suggest that the SF-protease releases cells from tissue in a way that ensures the continuity of the plasma membrane and cuts through the transmembrane attachment systems (either cell-cell or cell-extracellular matrix) without compromising the cytoskeletal integrity underlying native cell shape.

Animals↗
PubMedDate not supplied

[Structure, use, and risks of biomaterial repositories of embryonal tumors].

Availability of statistically sufficient numbers of tumor samples and other biomaterials in high quality together with corresponding clinical data is crucial for biomedical research. Tumor repositories from individual scientists are mostly not sufficient to satisfy these criteria, especially since pediatric tumors are rare. In 2000 three centralized tumor repositories (neuroblastoma in Cologne, nephroblastoma in Würzburg, hepatoblastoma, brain tumors in Bonn) have been established by the "German Competence Net Pediatric Oncology und Hematology". The aim was to collect biomaterial including tumor samples, normal tissue, and blood in high quality for research and diagnostic purposes at a central institution. Informed consent of the parents or patients is a prerequisite for scientific use of the samples and is requested by the therapy trial. The samples are collected according to accepted standards and shipped in the specially designed Tumorbox. The tumor repository organizes the distribution of the samples to the cooperating diagnostic laboratories. The number of collected tumor samples has increased over the years. In 2000, samples from 200 patients were collected while the patient number increased to 321 in 2005. Over the years the tumor repositories collected more than 7,150 samples (fresh frozen tumor, fresh frozen normal tissue, and blood). Through links with clinical trial databases the samples can be connected with clinical data. 12 of 14 applications for tumor material to be used in specific scientific projects have been approved by an independent supervisory board. The establishment of central tumor repositories represents a major step for biomedical research activities and quality control in pediatric oncology.

Biocompatible Materials↗
PubMed1988

pp60v-src tyrosine kinase is expressed and active in sarcoma-free avian embryos microinjected with Rous sarcoma virus.

Early embryonic avian tissue is resistant to transformation by Rous sarcoma virus. To determine the nature of this resistance, we examined the expression and properties of the Rous sarcoma virus transforming protein pp60v-src, in infected embryonic chicken limbs in ovo. Lysates from Rous sarcoma virus-infected limbs contained the viral structural protein p19gag, as detected by immunoblot analysis, and showed pp60v-src kinase activity in vitro. Immunoblot analysis of lysates with anti-phosphotyrosine antibodies revealed a number of phosphotyrosine-containing proteins present in lysates of Rous sarcoma virus-infected embryos but not in lysates of control, uninfected embryos. Anti-phosphotyrosine immunoreactivity was observed in frozen sections in the same cell types that expressed pp60v-src and p19gag. These studies demonstrate that pp60v-src is co-expressed with viral structural determinants in infected embryonic avian tissue. Furthermore, pp60v-src is active in ovo as a tyrosine-specific phosphotransferase, despite the apparent lack of sarcoma induction. The localization pattern of the major src gene substrate p36 (calpactin I) was compared with that of p19gag by double-label immunofluorescence and found to be generally nonoverlapping. These observations are consistent with the concept that the induction of tumors in ovo requires complementation between viral determinants and host factors. These host factors, which may be critical substrates of pp60v-src, are subject to developmental regulation in the avian embryo.

Animals↗