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  • 1980-1984  (4)
  • Chondrogenesis  (2)
  • Life and Medical Sciences  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 33 (1981), S. 425-430 
    ISSN: 1432-0827
    Keywords: Bone induction ; Insulin ; Chondrogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The influence of somatostatin on discrete stages of collagenous-matrix-induced endochondral bone formation has been investigated. Local injection of somatostatin, i.e., without any measurable systemic effect, resulted in a 75% reduction of cell proliferation as measured by [3H]thymidine incorporation and ornithine decarboxylase activities. The minimum effective inhibitory dose of somatostatin was 0.25 µg/day. Twice daily local injections of the hormone during cartilage formation also resulted in an inhibition, but this was shown to be due to impaired cell proliferation rather than to a direct effect of somatostatin on differentiation. Injection of somatostatin into developing bone tissue after the cartilage stage impaired osteogenesis, assessed by45Ca incorporation and alkaline phosphatase activity. Concurrent injections of insulin and somatostatin obliterated the inhibitory effect of the latter on cell proliferation. Somatostatin can locally regulate the proliferation and differentiation of chondroprogenitor and osteoprogenitor cells in vivo and may directly contribute to the regulation of bone growth by its ability to counteract the stimulatory effect of insulin.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 35 (1983), S. 732-739 
    ISSN: 1432-0827
    Keywords: Mesenchymol cell proliferation ; Chondrogenesis ; Osteogenesis ; Proteoglycans
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The influence of retinoic acid on matrix-induced endochondral bone differentiation was determined. Retinoic acid was administered during discrete stages of endochondral bone formation, specifically, mesenchymal cell proliferation, chondrogenesis, bone formation, and mineralization. In retinoic acid-treated rats examined on day 3 following matrix implantation, biochemical markers for mesenchymal cell proliferation were about 50% of the controls. Chondrogenesis on day 7, assessed by35SO4 incorporation into proteoglycans, was 27% of the control. In addition, dissociative extraction of proteoglycans with 4.0 M guanidine-HCl and chromatography on Sepharose CL-2B revealed the synthesis of a smaller molecular weight proteoglycan when compared to controls which exhibited the cartilage-specific type. Osteogenesis and bone mineralization were monitored by alkaline phosphatase activity and45Ca incorporation. On day 11 alkaline phosphatase activity was decreased by 40% and45Ca incorporation was 48% of the control. These results revealed the multiple foci of the actions of excess vitamin A.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 209 (1984), S. 21-27 
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Extracellular matrix is known to play an important role during development and maintenance of various tissues. In the present study, changes in two extracellular matrix glycoproteins, fibronectin and laminin, were investigated in skeletal muscle undergoing immune rejection. Purified antibodies against fibronectin and laminin were used to analyze the matrix by indirect immunofluorescence at various intervals after transplantation of extensor digitorum longus muscle in rats. Fibronectin and laminin were localized in the pericellular basement membrane zone of the normal myofibers; however, the cytoplasm was devoid of both glycoproteins. Transplanted muscle grafts underwent a process of degeneration and then an initial regeneration during the first 7 days. This regeneration effort ceased with the onset of muscle rejection in 14-day transplants. At this time, fibronectin was seen in the cytoplasmic region as well as the extracellular matrix of myofibers and myotubes. At later time intervals, an increased intensity of staining for fibronectin was seen throughout the rejected muscle. In muscle grafts undergoing regeneration but not rejection (i.e., nonantigenic grafts), such an increase in the presence of fibronectin was not seen (Gulati et al., 1982). The distribution of laminin did not change during the rejection process and was localized in the basement membrane zone of myofibers and myotubes, although the overall configuration of the basement membranes was deformed and collapsed. It appears that the basement membranes are resistant to degradation, and staining for laminin persists in rejected muscle. These results show marked changes in the extracellular matrix of muscle undergoing rejection. The appearance of fibronectin during the initial stages of muscle rejection may have a causal relationship to the process of immune defence mechanism; however, the exact role of fibronectin remains elusive.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 204 (1982), S. 175-183 
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The distribution of fibronectin in normal and regenerating skeletal muscle (the latter caused by autotransplantation) was investigated by means of indirect immunofluorescent technique. Normal myofibers exhibited a thin, continuous pericellular (endomysium) fibronectin distribution; however, their sarcoplasm was devoid of fibronectin. After autotransplantation, the skeletal muscle fibers underwent a process of degeneration that was followed by regeneration from the premyogenic satellite cells. These cells multiplied, fused to form myotubes, and matured into new myofibers. A decrease and an eventual loss of endomysial fibronectin was seen in the degenerating myofibers. At the same time, fibronectin appeared in the sarcoplasm. No significant fibronectin was expressed in the myogenic zone until the formation of myotubes which possessed a complete, circular fibronectin ring. The sarcoplasm of the myotubes lacked fibronectin. Since fibronectin is a component of basement membrane of several tissues, its disappearance and reappearance can be used to follow the fate of basement membrane. We conclude that fibronectin may not be essential for early myogenesis and that regenerated myotubes form an entirely new or at least certain new molecular components of their basement membrane. The present muscle autotransplantation model can be used to further study the role of fibronectin during myogenesis and cell transformation in vivo.
    Additional Material: 14 Ill.
    Type of Medium: Electronic Resource
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