Conflict of interest The authors state no conflict of interest.
Altered expression of dermokine in skin disorders
Version of Record online: 30 MAY 2012
© 2012 The Authors. Journal of the European Academy of Dermatology and Venereology © 2012 European Academy of Dermatology and Venereology
Journal of the European Academy of Dermatology and Venereology
Volume 27, Issue 7, pages 867–875, July 2013
How to Cite
Hasegawa, M., Higashi, K., Yokoyama, C., Yamamoto, F., Tachibana, T., Matsushita, T., Hamaguchi, Y., Saito, K., Fujimoto, M. and Takehara, K. (2013), Altered expression of dermokine in skin disorders. Journal of the European Academy of Dermatology and Venereology, 27: 867–875. doi: 10.1111/j.1468-3083.2012.04598.x
Funding sources This work was supported by grants from the Ministry of Education, Science and Culture of Japan.
- Issue online: 13 JUN 2013
- Version of Record online: 30 MAY 2012
- Received: 18 January 2012; Accepted: 7 May 2012
Background Although dermokine-β, a glycoprotein expressed in epithelial cells, does not have significant homology to other proteins, its carboxyl-terminal domain shares a high pI value with many cytokines, suggesting similar functions.
Objective To better understand the biology of dermokine, we here determined its localization under pathological conditions and examined factors that regulate its expression.
Methods We generated an anti-human dermokine-β/γ monoclonal antibody cross-reacting with the mouse protein. Using this antibody, immunohistological staining and Western blotting of dermokine-β/γ were performed with various tissue samples.
Results Although human dermokine-β/γ was expressed in almost all granular layers, upper spinous layers of the skin were also stained with anti-dermokine-β/γ antibody in inflammatory skin disorders. Dermokine-β/γ was expressed in keratoacanthoma and a part of well-differentiated squamous cell carcinoma (SCC). However, dermokine-β/γ was not detected in poorly differentiated SCC or tumours derived from non-keratinocytes. In mice, dermokine-β/γ-expressed keratinocytes were increased in models of contact hypersensitivity, ultraviolet-irradiated skin injury and wound healing. Consistent with expanded distribution in inflammatory skin diseases, proinflammatory cytokines such as interleukin-1β, interleukin-12, and tumour necrosis factor-α augmented dermokine-β/γ expression in cultured human keratinocytes. In contrast, growth factors including epidermal growth factor, insulin-like growth factor-I, keratinocyte growth factor and transforming growth factor-α significantly reduced dermokine expression.
Conclusion These results provide novel insights into the physiological and pathological significance of dermokine in the epidermis.