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Related Experiment Videos

UVB increases urokinase-type plasminogen activator receptor (uPAR) expression.

C Marschall1, E Lengyel, T Nobutoh

  • 1Department of Dermatology, Ludwig-Maximilians-Universität, München, Germany.

The Journal of Investigative Dermatology
|July 27, 1999
PubMed
Summary

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Ultraviolet B radiation increases urokinase-type plasminogen activator and its receptor in skin cells. This transcriptional response, mediated by an AP-1 binding site, may explain why pemphigus is worsened by sunlight.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Cell Biology

Background:

  • Keratinocytes produce urokinase-type plasminogen activator (uPA) and its receptor (uPAR).
  • The urokinase system is active in wound healing and pemphigus, an autoimmune skin disease.
  • Pemphigus lesions are sensitive to light, suggesting a role for UV radiation.

Purpose of the Study:

  • To investigate the effect of ultraviolet B (UVB) on uPA and uPAR expression in epidermal keratinocytes.
  • To elucidate the molecular mechanism of UVB-induced uPAR expression.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) for protein levels.
  • Flow cytometry for cell surface receptor expression.
  • Northern blot for mRNA analysis.

Related Experiment Videos

  • Reporter gene assays and electrophoretic mobility shift assays (EMSA) for transcriptional regulation.

    • Main Results:

    • UVB increased uPA protein and uPAR expression in A431 keratinocytes 24 hours post-irradiation.
    • UVB elevated uPAR mRNA levels with a delayed and prolonged response compared to epidermal growth factor.
    • UVB-induced uPAR expression was transcriptionally regulated via an AP-1 binding site in the promoter region.

    Conclusions:

    • UVB induces uPAR expression through a distinct transcriptional mechanism involving an AP-1 site.
    • The epidermal induction of the urokinase system by UVB may contribute to the photo-aggravation of pemphigus.
    • This study identifies a molecular link between UV exposure and the pathogenesis of pemphigus.