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Determining the Toxicity of UV Radiation and Chemicals on Primary and Immortalized Human Corneal Epithelial Cells
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Determining the Toxicity of UV Radiation and Chemicals on Primary and Immortalized Human Corneal Epithelial Cells

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[Effects of antisense epidermal growth factor receptor oligodeoxynucleotides on ultraviolet-induced c-jun activity of

Ji-Ping Xia1, Xiu-Zu Song, Wei-Ling Sun

  • 1Department of Dermatology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. Acta Academiae Medicinae Sinicae
|June 1, 2007
PubMed
Abstract

Insights

Antisense epidermal growth factor receptor (EGF-R) oligodeoxynucleotides effectively inhibit ultraviolet-induced c-jun activity in keratinocytes. This suggests EGF-R plays a key role in the cellular response to UV radiation.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Cell Biology

Background:

  • Ultraviolet (UV) radiation induces cellular responses in keratinocytes.
  • Epidermal growth factor receptor (EGF-R) signaling is implicated in cellular responses to stimuli.
  • c-jun is a transcription factor involved in cellular stress responses.

Purpose of the Study:

  • To investigate the role of EGF-R in ultraviolet-induced c-jun activity in keratinocytes.
  • To determine the effect of EGF-R antisense oligodeoxynucleotides on c-jun activity following UV exposure.

Main Methods:

  • Keratinocytes (HaCaT cell line) were transfected with EGF-R antisense oligodeoxynucleotides.
  • Ultraviolet-B (UVB) irradiation was applied to assess cellular response.
  • c-jun DNA binding activity was measured using a colorimetric assay.
  • EGF-R mRNA levels were quantified via reverse transcription polymerase chain reaction (RT-PCR).

Main Results:

  • UVB irradiation significantly increased c-jun activity in a dose-dependent manner.
  • Transfection with EGF-R antisense oligodeoxynucleotides inhibited UVB-induced EGF-R mRNA expression.
  • EGF-R antisense oligodeoxynucleotides significantly suppressed UVB-induced c-jun activity.

Conclusions:

  • UV-induced c-jun activity in keratinocytes is mediated by EGF-R.
  • EGF-R antisense oligodeoxynucleotides can effectively inhibit UV-induced c-jun activity.
  • Lipofectamine facilitates the transfection of EGF-R antisense oligodeoxynucleotides into keratinocytes.

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