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The scaffold protein JLP plays a key role in regulating ultraviolet B-induced apoptosis in mice

Radnaa Enkhtuya1, Tokiharu Sato, Mitsuo Wakasugi

  • 1Division of Molecular Cell Signaling, Cancer Research Institute, Kanazawa University, Kanazawa, 920-1192, Japan.

Genes to Cells : Devoted to Molecular & Cellular Mechanisms
|February 14, 2014
PubMed

Insights

J-like protein (JLP) prevents skin cell death from UVB radiation by regulating p38 MAPK signaling. This discovery reveals JLP

Area of Science:

  • Dermatology
  • Molecular Biology
  • Cell Biology

Background:

  • Ultraviolet B (UVB) radiation from sunlight damages skin cells and can lead to skin cancer.
  • UVB-induced signaling networks are complex, involving multiple cellular processes.
  • The role of J-like protein (JLP) in UVB responses is not well understood.

Purpose of the Study:

  • To investigate the role of J-like protein (JLP) in UVB-induced apoptosis in skin cells.
  • To elucidate the molecular mechanisms by which JLP influences UVB responses.

Main Methods:

  • Utilized Jlp knockout (KO) and keratinocyte-specific Jlp KO mice.
  • Assessed UVB-induced epidermal apoptosis and DNA damage repair.
  • Analyzed p38 mitogen-activated protein kinase (MAPK) activation in response to UVB.
  • Administered p38 inhibitor to UVB-irradiated wild-type and Jlp KO mice.

Main Results:

  • UVB-induced skin epidermal apoptosis was significantly reduced in Jlp KO mice.
  • JLP was not involved in the repair of UVB-induced DNA damage.
  • UVB-stimulated p38 MAPK activation was impaired in Jlp KO mice.
  • p38 inhibitor suppressed UVB-induced apoptosis in wild-type but not Jlp KO mice.

Conclusions:

  • J-like protein (JLP) in skin basal keratinocytes plays a critical role in UVB-induced apoptosis.
  • JLP modulates p38 MAPK signaling pathways, contributing to UVB-induced cell death.
  • This study is the first to demonstrate a crucial role for JLP in an in vivo response to environmental stimuli like UVB radiation.

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