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J. Biol. Chem., Vol. 282, Issue 8, 5834-5841, February 23, 2007

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Kallikrein 8 Is Involved in Skin Desquamation in Cooperation with Other Kallikreins^*

Mari Kishibe, Yoshio Bando, Ryuji Terayama, Kazuhiko Namikawa, Hidetoshi Takahashi, Yoshio Hashimoto, Akemi Ishida-Yamamoto, Ying-Ping Jiang^¶, Branka Mitrovic^¶, Daniel Perez^¶, Hajime Iizuka, and Shigetaka Yoshida¹

From the Departments of Structural Anatomy and Neuroscience and Dermatology, Asahikawa Medical College, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Japan and the ^¶Department of Immunology, Berlex Biosciences, Richmond, California 94804-0099

Kallikrein type serine proteases, KLK8/neuropsin, KLK6, and KLK7, have been implicated in the proliferation and differentiation of epidermal keratinocytes and in the pathogenesis of psoriasis. However, their mechanistic roles in these processes remain largely unknown. We applied 12-O-tetradecanoylphorbol-13-acetate on the wild type (WT) and the Klk8 gene-disrupted (Klk8^-/-) mouse skin, inducing keratinocyte proliferation similar to the human psoriatic lesion. Klk8 mRNA as well as Klk6 and Klk7 mRNA were up-regulated after 12-O-tetradecanoylphorbol-13-acetate application in the WT mice. In contrast, Klk8^-/- mice showed minimum increases of Klk6 and Klk7 transcripts, the proteins, and enzymatic activities. Relative to the WT, the Klk8^-/- skin showed less proliferation and an increase in the number of cell layers in the stratum corneum. However, overexpression of Klk8 by adenovirus vector in knock-out keratinocytes did not result in an increase in Klk6 or Klk7 mRNA. The inefficient cleavage of adhesion molecules DSG1 and CDSN in Klk8^-/- skin contributes to a delay in corneocyte shedding, resulting in the hyperkeratosis phenotype. We propose that in psoriatic lesion, KLK8 modulates hyperproliferation and prevents excessive hyperkeratosis by shedding the corneocytes.

Received for publication, August 21, 2006 , and in revised form, December 18, 2006.

^* This work was supported by grants from the Ministry of Education, Science, Culture and Sports, the Akiyama Foundation, and Inamori. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement"in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed. Tel.: 81-166-68-2300; Fax: 81-166-68-2309; E-mail: syoshida{at}asahikawa-med.ac.jp.

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