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Updated: May 19, 2026

Studying Chronic Exposure of Mice to Ultraviolet B Radiation
03:20

Studying Chronic Exposure of Mice to Ultraviolet B Radiation

Published on: August 19, 2025

Ultra-violet B (UVB)-induced skin cell death occurs through a cyclophilin D intrinsic signaling pathway

Chao Ji1, Bo Yang, Zhi Yang

  • 1Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210024, Jiangsu, China.

Biochemical and Biophysical Research Communications
|August 16, 2012
PubMed

Insights

Cyclophilin D (Cyp-D) plays a key role in UVB-induced skin cell damage by opening the mitochondrial permeability transition pore (mPTP). Inhibiting Cyp-D protects skin cells from UVB and oxidative stress, suggesting therapeutic potential.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Cell Biology

Background:

  • UVB radiation causes skin cell damage via mitochondrial permeability transition pore (mPTP) opening.
  • Cyclophilin D (Cyp-D) is crucial for mPTP opening and subsequent cell death.
  • Oxidative stress is implicated in skin damage pathways.

Purpose of the Study:

  • To investigate the role of Cyclophilin D (Cyp-D) in UVB and oxidative stress-induced skin cell death.
  • To determine if targeting Cyp-D can protect skin cells from damage.

Main Methods:

  • Western-Blot analysis to assess Cyp-D expression in human skin keratinocytes and HaCaT cells.
  • Generation of Cyp-D deficient keratinocytes using lentiviral shRNA.
  • Treatment with UVB, hydrogen peroxide (H(2)O(2)), N-acetyl cysteine (NAC), and cyclosporine A (Cs-A).
  • Over-expression of Cyp-D in primary keratinocytes.

Main Results:

  • UVB and H(2)O(2) increased Cyp-D expression, which was reduced by NAC.
  • Cyp-D deficient cells showed reduced susceptibility to UVB/H(2)O(2)-induced death.
  • Cs-A, a Cyp-D inhibitor, protected cells from UVB/H(2)O(2) induced death.
  • Cyp-D over-expression led to spontaneous keratinocyte cell death.

Conclusions:

  • Cyp-D is a critical mediator of UVB and oxidative stress-induced skin cell death.
  • Inhibition of Cyp-D offers a protective mechanism against skin cell damage.
  • Targeting Cyp-D presents a potential therapeutic strategy for managing skin damage.

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