bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anterior endoderm is a specific effector of terminal cardiac myocyte differentiation of cells from the embryonic heart forming region
Authors: Sugi Yukiko , Lough John 
Published: February 2005

AbstractThe ability of anterior lateral plate mesoderm cells in the heart‐forming region (HFR) of stage 6 chicken embryos to respond to cardiogenic stimuli from cells in adjacent germ layers has been investigated using explants cultured under defined conditions. Two types of explantation were evaluated: those in which two germ layers were explanted in contiguity, and those in which germ layers were isolated and co‐cultured. Two parameters—contractility and expression of sarcomeric alpha‐actin—were monitored to evaluate the terminal differentiation of cardiac myocytes. Contiguously explanted anterior endoderm/mesoderm became multilayered and underwent terminal differentiation within 2 days. By contrast, although contiguous anterior ectoderm/mesoderm or posterior endoderm/mesoderm co‐explants also became multilayered, these explants did not differentiate, up to 5 days. To ascertain the cardiogenic potential of cells from different regions of the embryo, individual germ layers were isolated and co‐cultured by placing the explants in separate areas of the culture chamber. These determinations demonstrated that anterior, but not posterior, endoderm effected differentiation of anterior mesoderm. As before, mesoderm in both types of co‐culture survived and became multilayered; by contrast, mesoderm did not survive when cultured in isolation. These experiments provide evidence that anterior endoderm regulates the terminal differentiation, as opposed to growth, of presumptive cardiac myocytes in mesoderm cells from the anterior lateral plate. Finally, anterior endoderm was co‐cultured with mesoderm from the posterior half of the embryo, which does not contain an HFR. The failure of these co‐cultured explants to differentiate infers that pre‐cardiac myoblasts in stage 6 anterior mesoderm are previously specified to respond to the terminal cardiogenic effects of endoderm. © 1994 Wiley‐Liss, Inc.
Growth dynamics of pancreatic islet cell populations during fetal and neonatal development of the rat
Authors: Kaung Hue‐lee Cheng 
Published: February 2005

AbstractRats from 18 days fetal to 28 days neonatal ages were studied for the total population sizes and cell proliferation activities of insulin secreting B cells, glucagon secreting A cells, somatostain secreting D cells, and pancreatic polypeptide secreting PP cells. Cell population sizes were assessed by morphometric quantitation of immunohistochemically stained cells by a linear scanning method and cell proliferation activities were estimated by [3H]‐thymidine labeling indices of these cell populations. There was a continuous increase in population sizes for all 4 islet cell types, with the fastest increase occurring in the last 4 days of gestation. The accelerated growth of these islet cell populations during late gestation was accomplished by a high cell proliferative activity at 20–22 days of gestation and a large influx of undifferentiated epithelial cells differentiating into the specific islet cell populations during this period. There was a reduction of population growth and cell proliferation for all islet cell types during the first 3–4 days of life. Growth activities continued for all islet cell populations after the 4th postnatal day, with a renewed acceleration in growth activities for B and A cells at this time. After the 10th neonatal day, the cell proliferation and total population growth continued at slow rates for all 4 islet cell types. The contribution from undifferentiated epithelial cells into the specific islet cell populations was negligible for B and A cells but continued at a low rate for PP and D cells during the first 10 days after birth. For B and A cell populations, there was a possibility that some cell loss occurred during the first 10 days of neonatal life. These dynamic changes of the growth characteristics provide a basis for understanding the abnormal growth of the endocrine pancreas. © 1994 Wiley‐Liss, Inc.
Control of somitic expression of tenascin in Xenopus embryos by myogenic factors and Brachyury
Authors: Umbhauer M. , Riou J.‐F. , Smith J. C. , Boucaut J. C. 
Published: February 2005

AbstractTenascin is a large glycoprotein which is expressed in a restricted pattern in the extracellular matrix (ECM) of vertebrate embryos. Tenascin interferes with cell‐fibronectin interactions in vitro, and may play a role in the control of cell migration and differentiation during development. In Xenopus, tenascin immunoreactivity is first detected at the early tailbud stage in the ECM of the most anterior somite. Thereafter, it is distributed dorsally along neural crest cell migration pathways. In this paper, we report that tenascin mRNA is most abundant in dorsal mesoderm at the neurula stage and in somites at the early tailbud stage, indicating that the initial accumulation of tenascin in the ECM is due to secretion from paraxial mesoderm. To understand how tenascin expression in somitic mesoderm is controlled, we have expressed Xbra and the myogenic factors XMyoD and XMyf5 in blastula animal cap tissue. The tenascin gene is activated by all three transcription factors. Interestingly, expression of tenascin mRNA, and accumulation of the protein in the ECM, can occur without formation of muscle. Our results suggest that tenascin regionalization in early Xenopus embryos depends on tenascin RNA expression by somitic mesoderm, where it is likely to be activated by myogenic factors. © 1994 Wiley‐Liss, Inc.
Type II collagen is transiently expressed during avian cardiac valve morphogenesis
Authors: Swiderski Ruth E. , Daniels Karla J. , Jensen Karen L. , Solursh Michael 
Published: February 2005

AbstractWe present new evidence of the temporal and spatial expression of type II collagen in the embryonic chick heart during the very early stages of its development. In particular, we emphasize the distribution of its mRNA and protein during valve formation. Type II collagen as well as several other fibrillar collagens (types I, III, and V) are present in stage 18 endocardial cushion mesenchymal cells. At stage 23, α1(II) collagen transcripts and the cognate polypeptide co‐localize in the atrioventricular valves. As development proceeds, the relative abundance of α1(II) collagen transcripts decreases during the stages studied (stages 22 to 45; day 3.5 to day 19) as assayed by RNA blotting of extracts of whole hearts. Type II collagen protein was immunologically undetectable in stage 38 (day 12) hearts, although collagens I, III, and V persisted and localize in the valve regions, in the endothelial lining of the heart, and in the epicardium. In keeping with other observations of type II collagen expression in non‐chondrogenic regions of a variety of vertebrate embryos, the avian heart also exhibits transient type II collagen expression. © 1994 Wiley‐Liss, Inc.
Developmental regulation of M‐cadherin in the terminal differentiation of skeletal myoblasts
Authors: Pouliot Yannick , Gravel Michel , Holland Paul C. 
Published: February 2005

AbstractCadherins form a large family of membrane glycoproteins which mediate homophilic calcium‐dependent cell adhesion. They are thought to mediate the initial calcium‐dependent cell adhesion which precedes the plasma membrane fusion of skeletal myoblasts. Two cadherin subtypes are known to be expressed in mammalian skeletal myoblasts: muscle cadherin (M‐cadherin) and neural cadherin (N‐cadherin). In the present study we demonstrate that (1) the expression of M‐ and N‐cadherin is differentially regulated during myoblast differentiation in vitro, (2) the expression of M‐cadherin but not N‐cadherin is inhibited by 5‐bromo‐2′‐deoxyuridine (BUdR), an agent which selectively inhibits skeletal myoblast differentiation, and (3) fusion and differentiation‐competent rat L6 myoblasts do not express detectable levels of N‐cadherin mRNA. In vivo, M‐cadherin mRNA was detectable exclusively in skeletal muscle. M‐cadherin mRNA levels peaked during the secondary myogenic wave in rat hindlimb muscle, becoming barely detectable in 1‐week‐old and adult rats. These observations indicate that M‐cadherin is unique in two ways: It is the first cadherin to be included in the family of skeletal muscle‐specific genes, and its shows peak leels of expression in developing skeletal muscle tissue. Taken together, these results suggest that M‐cadherin plays an important role in skeletal myogenesis. © 1994 Wiley‐Liss, Inc.
Developmental regulation of fatty acid binding protein in neural tissue
Authors: Sellner Peggy 
Published: February 2005

AbstractFatty acid binding proteins (FABP) constitute a family of small, cytosolic carriers of hydrophobic ligands. These proteins are thought to be important for lipid trafficking toward specific metabolic pathways, and are potentially important for the establishment of characteristic lipid compositions of neural tissue. In the embryonic chick retina and brain, FABP resembles the heart subtype, as determined by protein characterization and immunoblot studies. In this paper, the developmental expression and cellular localization of chick retinal FABP were examined. Results of immunoblot analysis suggest that FABP is maximally expressed around embryonic day 9 (E9) and declines thereafter. In adult retinas, FABP is barely detectable on a Western blot. Immunohistochemical staining of the retina shows light labeling on day E6 and a more intense staining throughout the retina on day E9. As the retina differentiates, labeling becomes increasingly localized. By day E18 subpopulations of ganglion cells and photoreceptor inner segments are stained, as are all photoreceptor cell bodies, most of the inner nuclear layer, and the nerve fiber layer. Staining is decreased in older retinas such that in adult animals, only light staining of the photoreceptor cell bodies is visible. The decrease in relative amount of FABP in the retina after day E9 suggests a role for FABP in the early stages of retinal differentiation. Localization in the retina is consistent with this hypothesis, as label becomes more restricted to those cells undergoing maturation at a particular developmental age. Thus, in young embryos (E6–E9), FABP immunolabeling is apparent throughout the retina, and transiently localizes at different ages (E12–E15) to plexiform and nuclear layers. Near hatching (E18–E21), the photoreceptors are in the final stages of maturation, and are the principal cells immunoreactive for FABP. In the adult retina, FABP lightly labels only the photoreceptor cells bodies; thus, we conclude that chick retinal FABP is not involved in outer segment membrane homeostasis. Instead, FABP may serve to sequester fatty acids needed for the period of neurite outgrowth which occurs as the retina ends its mitotic cycles and begins the process of synaptogenesis. © 1994 Wiley‐Liss, Inc.
Demethylation in the 5′‐flanking region of mouse cellular retinoic acid binding protein‐I gene is associated with its high level of expression in mouse embryos and facilitates its induction by retinoic acid in P19 embryonal carcinoma cells
Authors: Wei Li‐Na , Lee Chih‐Hao 
Published: February 2005

AbstractThe mouse cellular retinoic acid binding protein‐I (CRABP‐I) gene is specifically up‐regulated by retinoic acid (RA) in P19 mouse embryonal carcinoma cells, and its expression in animals is spatially and temporally restricted to RA‐sensitive tissues during embryonic development. This study demonstrates that, in adult mouse tissues and P19 cells where the expression of CRABP‐I is detected at the basal level, the 5′‐ flanking region of the CRABP‐I gene is hypermethylated at the C residues of all the Hpa II sites. Conversely, in mouse embryos during early stages of development when the expression of CRABP‐I gene is detected at a much higher level, this region is demethylated at these Hpa II sites. In P19, enhancement on the RA‐induced up‐regulation of CRABP‐I can be observed in cells treated with 5‐azacytidine (5‐AzaC) in conjunction with RA, where partial demethylation in the 5′‐flanking region of CRABP‐I gene is observed. Nuclear run‐on experiments indicate that increased message levels of CRABP‐I in P19 cells can be accounted for, at least partially, by increases in its transcription rates. The induction of retinoic acid receptor (RAR) β by RA can also be enhanced by 5‐AzaC, but to a much lesser degree. In contrast, all the Hpa II sites in the structural gene portion, at least in the first two exons, are fully demethylated at the C residues. © 1994 Wiley‐Liss, Inc.
Abnormal development of embryonic and extraembryonic cell lineages in parthenogenetic mouse embryos
Authors: Sturm Karin S. , Flannery Margaret L. , Pedersen Roger A. 
Published: February 2005

AbstractParthenogetically activated, diploid mouse oocytes can develop to midgestation stages in utero. However, even these advanced parthenogenones appear to die because of much reduced trophoblast and yolk sac development. Previous studies have compared the general features of parthenogenetic and androgenetic development and determined the fate of uniparental cells in chimeras with normal embryos. These studies led to the concept of genomic imprinting as the cause for developmental failure when either the maternal or the paternal genome is duplicated, with the corresponding deficiency of the other. Genomic imprinting appears to arise during gametogenesis and to act through dosage effects in a set of imprinted genes, whose expression depends on their parental origin. In this study we undertook a more detailed morphological analysis of parthenogenetic development in the mouse and established a classification system to quantify the developmental extent of parthenogenones. We found that the failure of parthenogenones occurred at different times during early postimplantation development, generating a spectrum of concepti which had developed to different extents, with only a small fraction of the embryos reaching advanced somite stages. In all parthenogenones differentiation and proliferation of the trophectoderm and primitive endoderm lineages (both extraembryonic) was abnormal, and in all, even the best‐developed parthenogenones, we observed similar deficiencies in the embryonic lineages, especially the mesoderm. Common to all abnormally developed lineages was that the proportion of undifferentiated precursor cells was much reduced, while their differentiated descendants were relatively abundant. We propose, therefore, that the failure of parthenogenones to develop to term is due to abnormal regulation of differentiation and proliferation in both embryonic and extraembryonic lineages. In this hypothesis, the apparent tissue specific defects observed in parthenogenones arise as a consequence of the functional importance of certain tissues (like the trophoblast) early in development. The spectrum of parthenogenones thus appears to reflect critical events in early development, whose regulation are affected by genomic imprinting. © 1994 Wiley‐Liss, Inc.
In vitro analysis of the spatial organization of chondrogenic regions of avian mandibular mesenchyme
Authors: Langille Robert M. 
Published: February 2005

AbstractThe mechanism(s) which control patterning in the face remain elusive, due in large part to the absence of morphologically identifiable controlling regions such as the AER of the limb bud. In order to identify the controlling region(s) and timing of patterning in the face, an investigation was launched to determine the spatial organization of tissues within this region, beginning with the chondrogenic zones of the avian (chick and quail) mandible. The mandibles from HH stage 23/24 chick and equivalent stage quail embryos were initially bisected in three planes giving rostral or caudal, proximal or distal, and medial or lateral halves. The mesenchyme from these various regions was isolated, plated out in high density micromass cultures, and grown for 4 days. Additionally, further cultures were grown, consisting of mandibular mesenchyme subdivided into quarters along the long axis of the mandible (e.g., rostro‐proximal quarter) as well as the bisecting of medial or lateral halves (e.g., medialrostral quarter). Nodule number and area were determined by morphometric analysis for each culture as well as whole mandible controls. The demarcation between chondrogenic and non‐chondrogenic regions was dramatic. Of the bisected halves, proximal and lateral were the most chondrogenic with the lateral subdivision displaying much more cartilage than whole mandible. The nodules of the lateral cultures fused into a sheet of cartilage. In constrast mesenchyme from the medial half was virtually non‐chondrogenic. When ranked by the amount of chondrogenesis, the order was, lateral > proximal = whole = core > distal > caudal > rostral > periphery ≫ medial. Interestingly, when subdivided further an altered pattern appeared. For example, the rostromedial quarter displayed a sheet of cartilage; more than the disto‐lateral or even the proximolateral which, based on the bisected‐mandible data, should have yielded the most cartilage. One possible explanation for the variance in the cartilage produced by the quartered mandibles from the amount predicted by the bisected‐mandible data is that further isolating portions of the mesenchyme changed the ratios of other cell types in the cultures and that cell‐cell interactions affect chondrogenic differentiation as suggested for limb mesenchyme. © 1994 Wiley‐Liss, Inc.
Differential expression of laminin isoforms and α6‐β4 integrin subunits in the developing human and mouse intestine
Authors: Simon‐Assmann Patricia , Duclos Brigitte , Orian‐Rousseau Véronique , Arnold Christiane , Mathelin Carole , Engvall Eva , Kedinger Michèle 
Published: February 2005

AbstractThe intestinal tissue is characterized by important morphogenetic movements during development as well as by a continuous dynamic crypt to villus epithelial cell migration leading to differentiation of specialized cells. In this study, we have examined the spatio‐temporal distribution of laminin A and M chains as well as of α6 and β4 integrin subunits in adult and developing human and mouse intestine by indirect immunofluorescence. Selective expression of the constituent polypeptides of laminin isoforms (A and M chains) was demonstrated. In the mature human intestine, A and M chains were found to be complementary, the M chain being restricted to the base of crypts and the A chain lining the villus basement membrane. In the developing human intestine, M chain expression was delayed as compared to that of A chain; as soon as the M chain was visualized, it exhibited the typical localization in the crypt basement membrane. A somewhat different situation was found in the adult mouse intestine, since both M and A chains were found in the crypts. During mouse intestinal development the delayed expression of the M chain as compared to that of the A chain was also obvious. The absence of M chain expression in mutant dy mouse did not impair intestinal morphogenesis nor cell differentiation. The expression of α6 and β4 subunits was not coordinated. In both species the α6 expression preceded that of β4. Furthermore, while β4 staining in adult mouse intestine was detected at the basal surface of all cells lining the cryptvillus, that of α6 was mainly confined to the crypt cell compartment. An overall similarity of location between α6 integrin subunit and laminin A chain at the epithelial/stromal interface was noted. These data indicate that the spatial and temporal distribution of laminin variants in the developing intestine may be characteristic for each species and that interactions of laminin variants with particular receptors may be important for induction and/or maintenance of differentiated cells. © 1994 Wiley‐Liss, Inc.
αv Integrin subunit is predominantly located in nervous tissue and skeletal muscle during mouse development
Authors: Hirsch Emilio , Gullberg Donald , Balzac Fiorella , Altruda Fiorella , Silengo Lorenzo , Tarone Guido 
Published: February 2005

Abstractαv integrin subunit can dimerize with different β subunits to form receptors for several matrix proteins. The function of these receptors in vivo is still largely unknown. We examined the localization of αv integrin during mouse development and showed that its distribution is dynamically regulated in the glia of the central nervous system and in skeletal muscle. Immunoreactivity in the neural tube was firstly localized at embryonic day 10.5 (E10.5) around cell bodies lining the lumen and along tiny fibers extending towards the outer margin. At E12.5 αv distribution follows the highly defined pattern of the radial glia: fascicles of immunoreactive fibres form parallel palisades, in particular along the hindbrain and the spinal cord. At E15.5, although with weaker intensity, αv was still detectable in radial glia fibres, and it codistributed with glial fibrillary acidic protein positive fascicles. After birth (P8) αv immunoreactivity in the brain and spinal cord decreased dramatically, but remained high in the radial glia of the cerebellum. In adult mice αv reactivity in the central nervous system disappeared. During myogenesis αv appears at E10.5 in myotomal cells and from E12.5 αv was evident in myoblasts and in myotubes. In the developing skeletal muscle of E15.5 embryos, immunoreactivity became more concentrated in the apical portion of the myotubes. In adult striated muscle the amount of αv subunit dramatically declined and immunostaining was no longer detectable. During development, αv was weakly evident in other sites including heart and endothelia of blood vessels, mesonephric tubula, smooth muscle of the digestive tract, and bronchia. Comparative analysis of the localization of αv, α3, and α5 integrin subunits indicated that αv has a unique and highly regulated distribution pattern. The distribution in the nervous system is consistent with a role of αv in neuron‐glia interaction during the organization of the neuronal layers in the brain cortex and in the cerebellum. Moreover, αv is likely to be involved in the myotendinous junction during embryonic life, suggesting a dual functional role of this integrin in muscle and nervous tissue. © 1994 Wiley‐Liss, Inc.
Structure and distribution of N‐cadherin in developing zebrafish embryos: Morphogenetic effects of ectopic over‐expression
Authors: Bitzur Sigal , Kam Zvi , Geiger Benjamin 
Published: February 2005

AbstractN‐cadherin cDNA was cloned from a zebrafish embryonic cDNA library. Analysis of the deduced amino acid sequence of this moleoule (ZN‐eadherin) revealed a high degree of homology to N‐cadherins of other species, except that its pre‐sequence is considerably shorter. Nevertheless, following transfection into chinese hamster ovary (CHO) cells, the expressed protein was functionally active, namely participated in calcium‐dependent intercellular interactions. Moreover, ectopic over‐expression of ZN‐cad‐herin, following mRNA microinjection into 2–4 cell embryos, caused microaggregation and uneven segregation of deep cells, resulting in distorted embryos. Developmental Northern and Western blot analyses indicated that both the mRNA and the protein first appear at gastrulation. In‐situ hybridization showed that ZN‐cadherin mRNA was initially present in all deep cells, and later became restricted to various epithelial and neural tissues. Whole‐mount immunostaining indicated that while ZN‐cadherin was already present at 50% epiboly, it became associated with cell junctions only 4–5 h later. In developing somites ZN‐cadherin expression was prominent but transient. High levels of the protein were detected in epithelial somites and its expression was apparently down regulated concomitantly with the onset of myogenesis. © 1994 Wiley‐Liss, Inc.