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Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage
12:59

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage

Published on: February 15, 2020

UVA1 radiation inhibits calcineurin through oxidative damage mediated by photosensitization

Ruben E A Musson1, Paul J Hensbergen, Adrie H Westphal

  • 1Department of Clinical Chemistry, Leiden University Medical Center, Leiden, The Netherlands. r.e.a.musson@lumc.nl

Free Radical Biology & Medicine
|March 1, 2011
PubMed

Insights

UVA1 radiation suppresses calcineurin activity by generating reactive oxygen species, offering a new understanding of skin signaling pathways. This finding links UVA1 effects to calcineurin inhibitors used therapeutically.

Area of Science:

  • Immunology
  • Dermatology
  • Biochemistry

Background:

  • Calcineurin is a key regulator of immune response, cellular development, and cell cycle.
  • It is a therapeutic target for allograft rejection and inflammatory skin conditions.
  • Calcineurin activity is modulated by reactive oxygen species and immunosuppressants.

Purpose of the Study:

  • To investigate the mechanism by which UVA1 radiation suppresses calcineurin activity.
  • To determine if other phosphatases are affected by UVA1 radiation.
  • To elucidate the molecular changes in calcineurin induced by UVA1.

Main Methods:

  • In vivo and in vitro experiments were conducted.
  • Reactive oxygen species (singlet oxygen and superoxide) were identified as mediators.
  • Protein phosphatase 2A (PP2A) was used as a control.
  • Mass spectrometry was used to analyze protein oxidation and conformational changes.

Main Results:

  • UVA1 radiation significantly suppresses calcineurin activity.
  • This suppression is mediated by singlet oxygen and superoxide generated via photosensitization.
  • PP2A activity remains unaffected.
  • Oxidation of methionine and cysteine residues and conformational changes in calcineurin were observed.

Conclusions:

  • UVA1 radiation inhibits calcineurin activity through oxidative damage.
  • The findings provide a mechanistic link between UVA1 radiation and calcineurin inhibitors.
  • This suggests a shared signaling pathway in skin affected by both UVA1 and calcineurin inhibitors.

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