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Gremlin inhibits UV-induced skin cell damages via activating VEGFR2-Nrf2 signaling

Chao Ji1, Jin-Wen Huang1, Qiu-Yun Xu1

  • 1Department of Dermatology, The First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, Fujian, China.

Oncotarget
|October 8, 2016
PubMed

Insights

Gremlin, a novel compound, protects skin cells from UV damage by activating VEGFR2 and Nrf2 signaling pathways, reducing cell death and DNA damage. This suggests gremlin

Area of Science:

  • Dermatology and Skin Biology
  • Molecular and Cellular Biology
  • Photobiology

Background:

  • Ultraviolet (UV) radiation causes skin damage through reactive oxygen species (ROS) production, DNA oxidation, and single-strand breaks (SSBs).
  • This damage can lead to skin cell demise and potentially skin cancer, necessitating protective strategies.

Purpose of the Study:

  • To investigate the potential of gremlin, a vascular endothelial growth factor receptor 2 (VEGFR2) agonist, in protecting skin cells against UV-induced damage.
  • To elucidate the underlying molecular mechanisms, specifically the involvement of VEGFR2 and NF-E2-related factor 2 (Nrf2) signaling.

Main Methods:

  • Utilized skin keratinocytes and fibroblasts exposed to UV radiation.
  • Assessed gremlin's effects on cell viability, apoptosis, ROS production, and DNA SSB formation.
  • Investigated the roles of VEGFR2 and Nrf2 using pharmacological inhibitors, shRNA knockdown, and dominant-negative mutations.

Main Results:

  • Gremlin significantly inhibited UV-induced skin cell death and apoptosis by activating VEGFR2.
  • Gremlin's cytoprotective effects were dependent on VEGFR2 activation and downstream signaling through Nrf2.
  • Gremlin markedly reduced UV-induced ROS production and DNA SSB formation in skin cells.

Conclusions:

  • Gremlin demonstrates significant cytoprotective activity against UV radiation in skin cells.
  • The protective mechanism involves the activation of the VEGFR2-Nrf2 signaling pathway.
  • Gremlin shows promise as a novel therapeutic agent for preventing UV-induced skin damage.
Keywords:
Nrf2VEGFR2gremlinskin cell damageultra violet (UV)

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