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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 277 (1984), S. 60-64 
    ISSN: 1432-069X
    Keywords: Histamine ; Collagen synthesis ; Fibroblasts
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Fibroblast-like cells derived from guinea-pig skin were cultured for 3 h in the presence of various concentrations of histamine. The total protein synthesized was determined by the incorporation of radioactive proline, and the collagenous protein synthesized was measured by the incorporation of labeled hydroxyproline in the cell layer and medium. Synthesis of both total and collagenous protein increased in the presence of histamine in the concentration range of 101–103 μg/ml. The ratio of collagen to total protein synthesized also increased at these concentrations. However, in no case was an increase found when H1 antagonist (chlorpheniramine) and H2 antagonist (cimetidine) were added with the histamine. DNA synthesis was not affected by histamine at the concentrations used. These results suggest that histamine increases the synthesis of collagen by fibroblast-like cells through H1 and H2-receptors.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 287 (1994), S. 115-121 
    ISSN: 1432-069X
    Keywords: Cytokines ; Fibroblasts ; Connective tissue ; Gene expression ; Tumour necrosis factor-α (TNF-α)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recently, the role of cytokines in controlling gene expression of connective tissue components has been increasingly emphasized. Many cytokines have been shown to have specific effects on gene expression of connective tissue components, and the roles of cytokines in controlling connective tissue metabolism during wound healing and in fibrosis have increasingly been discussed. In this article, the effects of cytokines on regulation of gene expression of connective tissue components, especially of type I collagen were described. We analysed transcriptional control of the α1(I) collagen gene by TNF-α by means of DNA mediated transfection experiments using recombinant plasmids in which the promoter region of the human α1(I) collagen had been fused to the chloramphenicol acetyl-transferase (CAT) gene, in human dermal fibroblasts. It was found that TNF-α reduced α1(I) collagen transcription through at least up to −107 bp upstream of the human α1(I) collagen promoter gene in dermal fibroblasts.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-069X
    Keywords: Key words In vitro aging ; Fibroblasts ; Type I collagen ; TGFβ ; TGFβ receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies have demonstrated that the expression of type I collagen, the most abundant protein in the dermis, is reduced in in vitro-aging fibroblast cultures, but the mechanism controlling the reduction of type I collagen expression is not understood. Recent studies, however, have demonstrated that transforming growth factor β (TGFβ) plays an important role in the regulation of type I collagen expression. The purpose of this study was to investigate the role of TGFβ in downregulation of type I collagen expression in in vitro-aged fibroblasts. We compared the expression of mRNA for α1(I) collagen, TGFβ ,TGFβ type I receptor and TGFβ type II receptor in early- and late-passage fibroblasts by Northern blot hybridizations. The mRNA levels of α1(I) collagen, TGFβ, and TGFβ receptors I and II in late-passage fibroblasts were reduced to 62%, 62%, 59% and 59%, respectively, of those in early-passage fibroblasts. We also compared TGFβ receptor binding in early- and late-passage fibroblasts using receptor binding assays. The affinity of   125 I-TGFβ in late-passage fibroblasts was lower than that in early-passage fibroblasts. These results suggest that the reduction of type I collagen expression in in vitro-aged fibroblasts is regulated by reduced expression of TGFβ and TGFβ receptors I and II and by decreased TGFβ receptor binding ability of the fibroblasts.
    Type of Medium: Electronic Resource
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