FEBS Letters
Volume 582, Issue 21 , Pages 3249-3253, 22 September 2008

Reciprocal regulation of 12- and 15-lipoxygenases by UV-irradiation in human keratinocytes

Edited by Sandro Sonnino

Laboratory of Dermato-Immunology, Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, Seoul 137-040, South Korea

Received 4 August 2008; received in revised form 19 August 2008; accepted 19 August 2008. published online 26 August 2008.

Abstract 

The 12/15-lipoxygenase (12/15-LOX) pathways of arachidonate metabolism have been implicated in the pathogenesis of psoriasis. Since UV photo-therapy is a commonly used technique for inhibiting cell proliferation and inflammation in skin diseases, we hypothesized that UV-irradiation may affect 12/15-LOX expression which might regulate cell proliferation. In this study, we showed that UV-irradiation suppressed 12-LOX expression, whereas up-regulated 15-LOX expression. Treatment with the 15-LOX metabolites sufficiently suppressed insulin-like growth factor II-induced 12-LOX expression and blocked cell cycle progression. On the basis of our findings, we think that the 15-LOX metabolites may inhibit epidermal hyperplasia in psoriasis by regulating 12-LOX expression.

Abbreviations: IGF-II, insulin-like growth factor II, 12/15-LOX, 12/15-lipoxygenase, PUVA, psoralen plus ultraviolet A

Keywords: 12/15-Lipoxygenase (LOX), HaCaT, IGF-II, Psoriasis, UV

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

PII: S0014-5793(08)00699-6

doi:10.1016/j.febslet.2008.08.017

FEBS Letters
Volume 582, Issue 21 , Pages 3249-3253, 22 September 2008