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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 126 (1992), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Collagen gene expression was studied in dermal fibroblasts derived from the inflammatory and sclerotic skin lesions of patients with localized or generalized morphoea. The levels of mRNA for type I collagen in early-passage fibroblasts derived from inflammatory lesions were higher than those obtained from the uninvolved skin, whereas those fibroblasts obtained from sclerotic lesions were unaltered. No alteration in type I collagen mRNA levels was observed in late-passage fibroblasts derived from the inflammatory lesions. The relative rate of collagen to total protein synthesis in earlypassage fibroblasts derived from inflammatory lesions was higher than that of fibroblasts from uninvolved skin, while no alteration or a slight decrease was observed in fibroblasts from the sclerotic lesions. The data suggest that the inflammatory reactions induce increased collagen synthesis by fibroblasts in the skin in scleroderma.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 284 (1993), S. 440-444 
    ISSN: 1432-069X
    Keywords: Tumor necrosis factor-α ; Normal fibroblasts ; Scleroderma fibroblasts ; Connective tissue metabolism ; Gene expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent studies have demonstrated that tumor necrosis factor-α(TNF-α) selectively decreases production of collagens I and III, the major types of collagen in the dermis, and increases production of collagenase in cultured dermal fibroblasts. The effects of TNF-α on collagens I, III and VI, fibronectin and collagenase gene expression by fibroblasts derived from normal individuals and patients with systemic sclerosis (SSc) were studied. SSc is characterized by excessive accumulation of collagen in the skin and in certain organs. TNF-α inhibited collagen production and mRNA levels of collagens I and III and of fibronectin, and stimulated collagenase activity and collagenase mRNA levels in SSs fibroblasts. Levels of mRNA for α1(VI) and α3(VI) collagen and for Β-actin were unaltered in SSc fibroblasts incubated with TNF-α. Similar results were observed for mRNA levels in normal fibroblasts incubated with TNF-α. These results suggest that TNF-α could be expected to be beneficial in the treatment of SSc. In addition, our results indicated that collagen-VI expression is regulated independently from expression of collagens I and III, and expression of fibronectin and collagens I and III are regulated in parallel in fibroblasts treated with TNF-α.
    Type of Medium: Electronic Resource
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  • 3
    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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