TRIM22 actives PI3K/Akt/mTOR pathway to promote psoriasis through enhancing cell proliferation and inflammation and inhibiting autophagy.
Cutan Ocul Toxicol
; 41(4): 304-309, 2022 Dec.
Article
em En
| MEDLINE
| ID: mdl-36170453
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-1ß, 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.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Psoríase
/
Fosfatidilinositol 3-Quinases
Limite:
Humans
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article