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  • Ingression  (1)
  • MATRIX METALLOPROTEINASES  (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
    Electronic Resource
    Electronic Resource
    Springer
    Journal of mammary gland biology and neoplasia 3 (1998), S. 215-225 
    ISSN: 1573-7039
    Keywords: BREAST CARCINOMA ; EXTRACELLULAR MATRIX ; LAMININ ; FIBROBLASTS ; MATRIX METALLOPROTEINASES ; IN VIVO TUMORIGENICITY
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The malignant progression of tumors is thoughtto be related to the expression of oncogenes and loss ofexpression of tumor suppressor gene. These factors areintrinsic to the cancer cells themselves. However, carcinomas are also infiltrated by host cells(fibroblasts, endothelial cells, inflammatory cells) andsurrounded by an extracellular matrix which isextensively remodeled. The extracellular matrixcomponents and infiltrating host cells provide amicroenvironment that conditions both tumor progressionand the metastatic process. Transplantation of humantumors into athymic nude mice has become an importantexperimental approach to study the biology of human cancers.The different models developed so far are beginning toelucidate the role of matrix molecules, growth factorsand enzymes as well as fibroblasts in tumor progression. These animal models are likely toprovide a useful tool to evaluate new antitumortreatments.
    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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