Cathepsin e induces itch-related response through the production of endothelin-1 in mice

Tsugunobu Andoh, Tetsuro Yoshida, Jung Bum Lee, Yasushi Kuraishi*

*この論文の責任著者

研究成果: ジャーナルへの寄稿学術論文査読

18 被引用数 (Scopus)

抄録

This study investigated the pruritogenic potency of cathepsin E, an aspartic protease, and its mechanisms in mice. An intradermal injection of cathepsin E to the rostral back elicited scratching, an itch-associated response, of the injection site. This action was inhibited by the aspartic protease inhibitor pepstatin A, the endothelin ET A receptor antagonist BQ-123, and the opioid receptor antagonists naltrexone and naloxone, but not by the H 1 histamine receptor antagonist terfenadine, the proteinase-activated receptor-2 antagonist FSLLRY-NH 2, or mast cell deficiency. Pepstatin A inhibited scratching induced by intradermal injection of the mast-cell degranulator compound 48/80, but not by tryptase, a mast-cell mediator. An intradermal injection of cathepsin E increased endothelin-1 levels in the skin at the injection site. Preproendothelin-1 mRNA was present in primary cultures of keratinocytes, and immunohistochemistry using an antibody recognizing endothelin-1 and big-endothelin-1 revealed immunoreactivity in the epidermis, especially in the prickle and granular cell layers, but not in the basal cell layer. These results suggest that cathepsin E is an endogenous itch inducer, and that its action is mediated at least in part by the production of endothelin-1 in the epidermis.

本文言語英語
ページ(範囲)16-21
ページ数6
ジャーナルEuropean Journal of Pharmacology
686
1-3
DOI
出版ステータス出版済み - 2012/07/05

ASJC Scopus 主題領域

  • 薬理学

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