Downregulation of 14-3-3β and 14-3-3ζ in lesions of psoriasis vulgaris

Authors


  • Conflict of interest: none declared.

Correspondence: Professor Xiaoyan Zhang, Department of Dermatology, China-Japan Friendship Hospital, Beijing, China

E-mail: manxhg@yahoo.com.cn

Summary

Background

The 14-3-3 proteins are a family of conserved regulatory molecules expressed in all eukaryotic cells, which play essential roles in a wide range of vital regulatory processes, including differentiation, proliferation and transformation. In mammalian cells, seven 14-3-3 isoforms (β, γ, ε, η, θ/τ, σ and ζ) have been identified, and each of these seems to have distinct tissue localizations and isoform-specific functions. 14-3-3β and 14-3-3ζ are two important members of the 14-3-3 family.

Aim

To explore the role of 14-3-3β and 14-3-3ζ in normal skin and psoriasis vulgaris (PV) skin.

Methods

Using immunohistochemistry and western blotting, we measured expression of 14-3-3β and 14-3-3ζ in 30 PV lesions and 15 normal skin samples. The average optical density (OD) of immunostaining and the relative grey scale of immunoblotting for 4-3-3β and 14-3-3ζ were analysed by the t-test.

Results

The average OD of immunostaining for 14-3-3β and 14-3-3ζ was 0.17 ± 0.00 and 0.24 ± 0.01, respectively, in psoriatic lesions, which was significantly lower than in normal controls (0.22 ± 0.01 and 0.37 ± 0.02, respectively; < 0.01 for both). There was also a significant difference in the relative grey scale of 14-3-3β and 14-3-3ζ (0.52 ± 0.03 and 1.44 ± 0.06, respectively) in psoriatic lesions compared with normal control tissue (3.32 ± 0.15 and 2.76 ± 0.11, respectively; < 0.01 for both).

Conclusions

Expression of 14-3-3β and 14-3-3ζ were lower in psoriatic lesions than in normal human skin tissue. We speculate that 14-3-3β and 14-3-3ζ may be involved in the regulation of normal skin function, thus decreased expression of 14-3-3β and 14-3-3ζ might precipitate the disturbance in proliferation and differentiation of keratinocytes seen in psoriasis.

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