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Related Experiment Videos

Factor XIII in scleroderma: in vitro studies.

M Paye1, D Read, B Nusgens

  • 1Laboratory of Experimental Dermatology, Tour de Pathologie, CHU du Sart Tilman, University of Liège, Belgium.

The British Journal of Dermatology
|March 1, 1990
PubMed
Summary
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Factor XIII (FXIII) benefits progressive systemic sclerosis (PSS) skin lesions. In vitro, FXIII reduces excessive collagen synthesis and increases its degradation by PSS fibroblasts.

Area of Science:

  • Dermatology
  • Biochemistry
  • Cell Biology

Background:

  • Progressive systemic sclerosis (PSS) is characterized by excessive collagen deposition in skin lesions.
  • Factor XIII (FXIII) administration shows a beneficial effect in approximately 50% of PSS patients.
  • The in vitro effects of FXIII on fibroblast function in PSS are not fully understood.

Purpose of the Study:

  • To investigate the in vitro effects of Factor XIII (FXIII) on the functions of normal and PSS skin fibroblasts.
  • To determine if FXIII can modulate the excessive collagen synthesis observed in PSS fibroblasts.

Main Methods:

  • Culturing normal and PSS skin fibroblast strains in vitro.
  • Assessing fibroblast functions including proliferation, attachment, collagen synthesis, and collagen degradation.

Related Experiment Videos

  • Treating fibroblast cultures with Factor XIII (FXIII) at a concentration of 1 U/ml.

    • Main Results:

    • Most PSS fibroblast strains exhibited excessive collagen synthesis in vitro.
    • FXIII significantly inhibited collagen synthesis in normal fibroblasts and reduced it in PSS fibroblasts to normal levels.
    • FXIII treatment led to increased degradation of newly synthesized collagen in PSS fibroblasts cultured in collagen lattices.
    • Other tested fibroblast functions, such as adhesion and proliferation, were not significantly affected by FXIII.

    Conclusions:

    • Excessive collagen production by PSS fibroblasts can be effectively repressed by FXIII in vitro.
    • FXIII exerts its effect through at least two mechanisms: reducing collagen synthesis and enhancing collagen degradation.
    • These findings suggest a potential therapeutic role for FXIII in managing excessive collagen deposition in PSS.