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  • 1
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 128 (1986), S. 322-328 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: We investigated the influence of transforming growth factor-β (TGF-β) on DNA synthesis in human fetal fibroblasts, as measured by the incorporation of [3H] thymidine and cell replication. In serum-free medium, without additional peptide growth factors, TGF-β had no action on thymidine incorporation. However, in the presence of 0.1% v/v fetal calf serum, TGF-β exhibited a bi-functional action on the cells. A dose-dependent stimulation of [3H] thymidine incorporation, and an increase in cell number, occurred with fibroblasts established from fetuses under 50 g body weight, with a maximum stimulation seen at 1.25 ng/ml. For fibroblasts from fetuses of 100 g or greater body weight, TGF-β caused a dose-related decrease in thymidine uptake with a maximal inhibition at 2.5 ng/ml, and a small decrease in cell number. When DNA synthesis was stimulated by the addition of somatomedin-C/insulin-like growth factor I, epidermal growth factor, or platelet-derived growth factor, their actions were potentiated by the presence of TGF-β on cells derived from fetuses under 50 g body weight, but inhibited on cells obtained from the larger fetuses wieghing more than 100 g. Similar results were found for changes in cell number in response to TGF-β when stimulated by SM-C/IGF I. The ability of TGF-β to modulate [3H] thymidine incorporation did not involve a change in the time required for growth-restricted cells to enter the S phase of the replication cycle. These data suggest that TGF-β may exert either a growth-promoting or growth-inhibiting action on human fetal connective tissues in the presence of other peptide growth factors, which is dependent on fetal age and development.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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