The EGFR-ERK/JNK-CCL20 pathway in scratched keratinocytes may underpin koebnerization in psoriasis patients

Kazuhisa Furue, Takamichi Ito, Yuka Tanaka, Akiko Hashimoto-Hachiya, Masaki Takemura, Maho Murata, Makiko Kido-Nakahara, Gaku Tsuji, Takeshi Nakahara, Masutaka Furue

研究成果: Contribution to journalArticle査読

5 被引用数 (Scopus)

抄録

Epidermal keratinocytes represent a rich source of C-C motif chemokine 20 (CCL20) and recruit CCR6+ interleukin (IL)-17A–producing T cells that are known to be pathogenic for psoriasis. A previous study revealed that scratch injury on keratinocytes upregulates CCL20 production, which is implicated in the Koebner phenomenon characteristically seen in psoriasis patients. However, the molecular mechanisms leading to scratch-induced CCL20 production remain elusive. In this study, we demonstrate that scratch injury upregulates the phosphorylation of epidermal growth factor receptor (EGFR) and that the specific EGFR inhibitor PD153035 attenuates scratch-induced CCL20 upregulation in an extracellular signal-related kinase (ERK)-dependent, and to a lesser extent, a c-Jun N-terminal kinase (JNK)-dependent but p38 mitogen-activated protein kinase (MAPK)–independent manner. Immunoreactive CCL20 was visualized in the keratinocytes that lined the scratched wound. IL-17A also induced the phosphorylation of EGFR and further augmented scratch-induced CCL20 upregulation. The EGFR-ERK/JNK-CCL20 pathway in scratched keratinocytes may explain why Koebnerization is frequently seen in psoriasis patients.

本文言語英語
論文番号434
ジャーナルInternational journal of molecular sciences
21
2
DOI
出版ステータス出版済み - 1 2 2020

All Science Journal Classification (ASJC) codes

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

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