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  • Artikel: DFG Deutsche Nationallizenzen  (1)
  • Endothelial cells  (1)
  • 1
    ISSN: 1432-5233
    Schlagwort(e): Diabetes mellitus ; Diabetic retinopathy ; Endothelial cells ; Growth factors ; Pericytes
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Pericytes disappear early, selectively and specifically from retinal capillaries in diabetic microangiopathy, but little is known of their growth and turnover in health and disease. We have studied the effects of human blood derivatives and of a panel of individual growth factors on [3H]thymidine incorporation in bovine retinal pericytes and endothelial cells. Human serum and platelet-rich plasma stimulated incorporation of the nucleotide in a dose-dependent manner in both cell types, and did so more potently than platelet-free plasma. Consistent and significant stimulation of DNA synthesis in pericytes was observed with basic fibroblast growth factor (ED50= 1.8×10−13 mol/l), acidic fibroblast growth factor (7.4× 10−12 mol/l), insulin-like growth factor 1 (8.6×10−10 mol/l), insulin (158 μU/ml) and endothelin-1 (6.1×10−10 mol/l). Transforming growth factor β1 inhibited DNA synthesis (ID50=3.6×10−10 mol/l) and so did heparin (1.4×10−6 mol/l) and low molecular weight heparin (2.9×10−6 mol/l). Retinal endothelial cells were stimulated by basic fibroblast growth factor (3.2×10−13 mol/l) and acidic fibroblast growth factor (1.3×10−9 mol/l), and inhibited by transforming growth factor β1, (1.6×10−12 mol/l). Neither cell type was stimulated by platelet-derived growth factor (A+B chain heterodimer), epidermal growth factor, growth hormone, or nerve growth factor (7S complex). The characteristics and active concentrations of the above growth factors suggest that none is solely responsible for the pericyte mitogenic activity of platelets, serum or plasma. Some, though, may play a role in the regulation of pericyte turnover through paracrine mechanisms which should be further investigated.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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