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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on November 25, 2002; DOI: 10.1124/jpet.102.044545

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Received for publication September 20, 2002.
Revised October 11, 2002.
Accepted for publication November 19, 2002.

Selective cyclooxygenase-2 inhibition does not alter keratinocyte wound responses in the mouse epidermis after abrasion

Medora M. Hardy 1*, Eric A.G. Blomme 1, Andrew R. Lisowski 1, Kevin S. Chinn 1, Amy L. Jones 1, Janet M. Harmon 1, Alan C. Opsahl 1, Richard L. Ornberg 1, Catherine S. Tripp 1

1 Pharmacia

* Address correspondence to: E-mail: medora.m.hardy{at}pharmacia.com

Abstract

The cyclooxygenase isoforms, COX-1 and COX-2, are the rate limiting enzymes in the biosynthesis of prostaglandin E2, a major prostaglandin involved in epidermal homeostasis and repair. Epidermal injury results in transient hyperplasia and induction of COX-2 expression. However, the role of COX-2 in this hyperplasia is unknown. In this study, we characterized the epidermal expression of COX isozymes following wounding by abrasion in SKH-1 mice using immunohistochemistry, in situ hybridization and Western analysis. In addition, we evaluated pivotal keratinocyte functions necessary for the reparative hyperplasia, including proliferation by BrdU labeling and differentiation by the expression of involucrin, keratin 1 and keratin 6. While COX-1 expression in keratinocytes remained unchanged during wound healing, COX-2 expression was induced coincidently with keratinocyte proliferation and keratin 6 expression, suggesting a role for COX-2 in epidermal repair. The role of COX-2 was also evaluated using the selective COX-2 inhibitor, SC-791, and the traditional COX inhibitors, indomethacin and diclofenac. Neither inhibitor altered keratinocyte proliferation or differentiation following abrasion, in contrast to dexamethasone, which delayed these responses. Our results indicated that, although COX-2 expression was coincident with transient epidermal hyperplasia and keratinocyte proliferation/differentiation during the healing of epidermal injury, it does not play a pivotal role in this repair process.


Key words: abrasion, cyclooxygenase-2, epidermis, healing, keratinocyte, wound


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