TRIM22 actives PI3K/Akt/mTOR pathway to promote psoriasis through enhancing cell proliferation and inflammation and inhibiting autophagy

Abstract

Objective

To reveal the function and underlying mechanism of Tri-domain protein 22 (TRIM22) in psoriasis.

Methods

M5 cytokines were applied in HaCat cells to mimic psoriasis in vitro. The TRIM22-silencing viruses were established to knockdown TRIM22 in HaCat cells. Western blot and/or real-time PCR were used to detect the expression of TRIM22, KRT1, KRT6, p-P65, P65, LC3, Beclin 1, P62, p-PI3K, PI3K, p-Akt, Akt, p-mTOR, and mTOR. ELISA kits were applied to assess levels of TNF-α, IL-1β, IL-18, and HMGB1.

Results

TRIM22 expression levels were upregulated in M5-treated HaCat cells. M5 treatment enhanced cell proliferation and inflammation, and inhibited autophagy in HaCat cells which were effectively reversed by TRIM22 deficiency. Activation of PI3K/Akt/mTOR pathway is an essential promoter of cell proliferation and inflammation, and inhibitor of autophagy in psoriasis. TRIM22 deficiency blocked M5-induced activation of PI3K/Akt/mTOR pathway in HaCat cells.

Conclusions

TRIM22 facilitates cell proliferation and inflammation, and suppresses autophagy in M5-treated HaCat cells through activating PI3K/Akt/mTOR pathway, and inhibition of TRIM22 can be a novel potential treatment for psoriasis.

Keywords:

• Tri-domain protein 22 (TRIM22)
• PI3K/Akt/mTOR pathway
• psoriasis

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

The authors declare that all data supporting the findings of this study are available within the paper and any raw data can be obtained from the corresponding author upon request.