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  • Gastrulation  (1)
  • MCF-7 breast cancer cells  (1)
  • Skin  (1)
  • 1
    ISSN: 1432-041X
    Keywords: Collagen ; Fibronectin ; Laminin ; Skin ; Scale morphogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Collagen types I and III were purified from the skin of 3-or 7-week-old chickens, collagen type IV from bovine skin or EHS mouse tumour, fibronectin from human serum, and laminin from EHS mouse tumour. Antibodies were produced in rabbits or sheep, and used in indirect immunofluorescence on frozen sections of 9-to 16-day-old normal or mutant (scaleless) chick-embryo foot skin. In normal scale-forming skin and inscaleless skin, the distribution of anti-laminin and anti-type IV collagen label was uniform along the dermal-epidermal junction and showed no stage-related variations, except for fluorescent granules located in the dermis of early scale rudiments. By contrast, in normal scale-forming skin, the density of anti-types I and III label decreased in the dermis within scale rudiments, whereas it gradually increased in interscale skin. Conversely, anti-fibronectin label accumulated at a higher density within scale rudiments than in interscale skin. In the dermis of thescaleless mutant, anti-types I and III label and antifibronectin label were distributed evenly: the density of anti-collagen label increased with age, while that of antifibronectin decreased and almost completely vanished in 16-day-old skin, except around blood vessels. The microheterogeneous distribution of some extracellular matrix components, namely interstitial collagen types I and III and fibronectin, is interpreted as part of the morphogenetic message that the dermis is known to transmit to the epidermis during the formation of scales. The even distribution of these components in mutantscaleless skin is in agreement with this view. Basement membrane constituents laminin and type-IV collagen do not appear to be part of the dermal morphogenetic message.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-7217
    Keywords: FGF-3 ; FGF-4 ; MCF-7 breast cancer cells ; tumorigenicity ; VEGF
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The transforming properties of fibroblast growth factor 3 (FGF-3) were investigated in MCF7 breast cancer cells and compared to those of FGF-4, a known oncogenic product. The short form of fgf-3 and the fgf-4 sequences were each introduced with retroviral vectors and the proteins were only detected in the cytoplasm of the infected cells, as expected. In vitro, cells producing FGF-3 (MCF7.fgf-3) and FGF-4 (MCF7.fgf-4) displayed an amount of estrogen receptors decreased to around 45% of the control value. However, MCF7.fgf-3 cell proliferation remained responsive to estradiol supply. The sensitivity of the MCF7.fgf-4 cells, if existant, was masked by the important mitogenic action exerted by FGF-4. In vivo, the MCF7.fgf-3 and MCF7.fgf-4 cells gave rise to tumors under conditions in which the control cells were not tumorigenic. Supplementing the mice with estrogen had the paradoxical effect of totally suppressing the start of the FGF-3 as well as the FGF-4 tumors. Tumorigenicity in the presence of matrigel was similar for MCF7.fgf-3 and control cells and was increased by estrogen supplementation. Once started, the MCF7.fgf-4 tumors grew with a characteristic high rate. Remarkably, FGF-4 but not FGF-3, stimulated the secretion of vascular endothelial growth factor (VEGF65) without altering the steady-state level of its mRNA, suggesting a possible regulation of VEGF synthesis at the translational level in MCF7 cells. The increased VEGF secretion is probably involved in the more aggressive phenotype of the MCF7.fgf-4 cells while a decreased dependence upon micro-environmental factors might be part of the increased tumorigenic potential of the MCF7.fgf-3 cells.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0003-276X
    Keywords: Mesoblast migration ; Ingression ; Gastrulation ; Chicken blastoderm ; Fibronectin ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The involvement of fibronectin in adhesion and migration of individual mesoblast cells during chicken gastrulation was examined after microinjection of functional and nonfunctional antifibronectin antibodies in the blastoderm during the period of rapid migration of mesoblast cells. The injection of affinity-purified polyclonal antihuman fibronectin antibody (total IgG or Fab fragment) or of monoclonal antichicken cellular fibronectin caused a thickening of the primitive streak, which was composed of loosely connected cells. This effect was most evident at the level of Hensen's node, and very few mesoblast cells were observed migrating in the space between upper layer and deep layer. The obvious explanation of this effect was that the de-epithelialization of upper layer cells persisted in the presence of antibodies, but ingressed cells failed to emigrate from the primitive streak. Immunostaining of microinjected antibodies showed binding to the basement membrane, to the cell surface of mesoblast cells that had migrated before microinjection occurred, and to the cell surface of deep layer cells. Cells that ingressed and detached in the course of reincubation of the embryo possessed little immunolabelling along their cell surface. The results suggest that the failure of ingressed cells to emigrate from the primitive streak and to form mesoblast was due (1) to alterations in adhesion between newly ingressed primitive streak cells, which had the ability to detach but possessed relatively little fibronecting along their cell surfaces and a small number of cell protrusions, and (2) probably to a lack of adhesion of detached cells to the basement membrane, which was blocked by the presence of antifibronectin antibodies. We conclude that the presence of fibronectin in the basement membrane is required for emigration of ingressed cells and migration of mesoblast cells to occur. Once migration has commenced, fibronectin is also deposited along the cell surface of migrating cells, a factor that may increase their mutual adhesion. © 1993 Wiley-Liss, Inc.
    Additional Material: 18 Ill.
    Type of Medium: Electronic Resource
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