Effect of interleukin-17 on receptor-interacting protein 4 expression and keratinocyte proliferation

Jia,Kun; Zhang,Yan; Ma,Weiyuan; Zhang,Xiaofeng; Sun,Qing

doi:10.3892/etm.2015.2478

Effect of interleukin-17 on receptor-interacting protein 4 expression and keratinocyte proliferation

Authors:
- Kun Jia
- Yan Zhang
- Weiyuan Ma
- Xiaofeng Zhang
- Qing Sun
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Affiliations: Shandong University School of Medicine, Jinan, Shandong 250012, P.R. China, Department of Dermatology, Qilu Hospital, Shangdong University, Jinan, Shandong 250012, P.R. China
Published online on: May 7, 2015 https://doi.org/10.3892/etm.2015.2478
Pages: 374-378

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Abstract

The aim of the present study was to investigate the effect of receptor-interacting protein 4 (RIP4) on keratinocyte proliferation and its role in the pathogenesis of psoriasis vulgaris. The expression of RIP4 and Ki‑67 in fixed sections from 30 patients with psoriasis vulgaris and 30 gender‑ and age‑matched healthy controls was detected by two‑step immunohistochemistry, prior to the correlation being examined with Pearson's analysis. Reverse transcription‑semi‑quantitative polymerase chain reaction and western blot analyses were carried out to detect the mRNA and protein expression of RIP4 in an immortalized human keratinocyte line, HaCaT, stimulated by different concentrations of interleukin‑17 (IL‑17), in order to analyze the change in RIP4 expression following IL‑17 stimulation. The cell proliferation rate was measured using the cell counting kit‑8 assay simultaneously. RIP4 was mainly present in the cytoplasm of the keratinocytes. Compared with its expression in the healthy control skin, RIP4 exhibited a significant upregulation in the psoriatic lesions (P<0.05). Pearson's correlation analysis revealed a positive correlation between the expression level of RIP4 and the proliferation index. Both RIP4 mRNA and protein levels were significantly increased following IL‑17 stimulation. Exposure to IL‑17 additionally increased the proliferation rate of the HaCaT cells. In conclusion, RIP4 may play a role in the pathogenesis of psoriasis vulgaris as a potential target of IL-17.

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