IL‑17 promotes proliferation, inflammation and inhibits apoptosis of HaCaT cells via interacting with the TRAF3 interacting protein 2

Zhang,Jie; Zhang,Junbin; Lin,Qingxia; Chen,Lamei; Song,Yali

doi:10.3892/etm.2020.9480

IL‑17 promotes proliferation, inflammation and inhibits apoptosis of HaCaT cells via interacting with the TRAF3 interacting protein 2

Authors:
- Jie Zhang
- Junbin Zhang
- Qingxia Lin
- Lamei Chen
- Yali Song
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Affiliations: Department of Dermatology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China, Department of Dermatology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250014, P.R. China, Department of Dermatology, Affiliated Hospital of Weifang Medical University, Weifang, Shandong 261000, P.R. China
Published online on: November 18, 2020 https://doi.org/10.3892/etm.2020.9480
Article Number: 49
Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study aimed to investigate the effects of interleukin‑17 (IL‑17) on the function of keratinocytes and to further investigate its associated mechanism. Human immortalized epidermal cells (HaCaT) were divided into sham control group (Sham), TRAF3 interacting protein 2 (TRAF3IP2)‑knockdown with lentivirus group (si‑TRAF3IP2), sham control+IL‑17 group (Sham+IL‑17) and TRAF3IP2‑knockdown with lentivirus+IL‑17 group (si‑TRAF3IP2+IL‑17). MTT and flow cytometry assays demonstrated that IL‑17 promoted proliferation and inhibited apoptosis of HaCaT cells, while this effect was reversed following knockdown of TRAF3IP2 with lentiviral vectors. In addition, a marked increase in the levels of IL‑6, IL‑8, IL‑23, TNF‑α and VEGF was observed in the Sham+IL‑17 group compared with that noted in the Sham group (P<0.05). Furthermore, reverse transcription‑quantitative polymerase chain reaction and western blotting indicated that the mRNA and protein expression levels of caspase‑3 in the si‑TRAF3IP2+IL‑17 group were significantly increased compared with those of the Sham+IL‑17 group (P<0.05). Taken together, the results indicated that IL‑17 promoted proliferation and inflammation and inhibited apoptosis of HaCaT cells by interacting with the TRAF3IP2 adaptor protein, while knockdown of the expression of TRAF3IP2 reduced the effects of IL‑17 in HaCaT cells.

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