Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor

Megan Landis, Qiaofang Yi, Ann Marie Hyatt, Angela R. Travers, Davina A. Lewis, Jeffrey B. Travers

Research output: Contribution to journalArticle

3 Scopus citations


Platelet-activating factor (PAF) is a group of phosphocholines with various biological effects, which are mediated by the PAF receptor (PAF-R). Our previous studies have demonstrated that ultraviolet B radiation (UVB) is a potent stimulus for PAF production, and that the presence of the PAF-R on epithelial cells results in an augmentation of UVB-induced apoptosis. Inasmuch as PAF-R activation results in numerous signal transduction pathways, the present study was designed to characterize the signal transduction pathway responsible for PAF-R-mediated enhanced UVB-induced cytotoxicity. Using a model system of PAF-R-negative and -positive epithelioid KB cells, we demonstrate that inhibitors of p38 MAP kinase block the augmentation of UVB-mediated apoptosis seen in PAF-R-positive KB cells. In contrast, pharmacological and/or molecular inhibition of other pathways linked to PAF-R activation including ERK MAP kinase and NFκB do not affect PAF-R-mediated cytotoxicity. This study demonstrates the important role that p38 MAP kinase plays in PAF-R-mediated augmentation of UVB cytotoxicity.

Original languageEnglish (US)
Pages (from-to)263-266
Number of pages4
JournalArchives of Dermatological Research
Issue number5-6
StatePublished - Aug 1 2007



  • Apoptosis
  • p38 MAP kinase
  • Platelet-activating factor
  • UVB

ASJC Scopus subject areas

  • Dermatology

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