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Circ_0060531 knockdown ameliorates IL-22-induced keratinocyte damage by binding to miR-330-5p to decrease GAB1 expression.
- Source :
-
Autoimmunity . Jun2022, Vol. 55 Issue 4, p243-253. 11p. - Publication Year :
- 2022
-
Abstract
- Psoriasis is a chronic immune-mediated skin disease. Recent studies showed its pathogenesis involved circular RNA (circRNA). However, the role of circ_0060531 in psoriasis development and the behind mechanism remain to be explored. Psoriasis cell model was constructed by treating keratinocytes (HaCaT cells) using interleukin 22 (IL-22). Expression of circ_0060531, microRNA-330-5p (miR-330-5p) and GRB2 associated binder 1 (GAB1) was determined by quantitative real-time polymerase chain reaction. The functional effects of circ_0060531 on IL-22-caused cell injury were investigated by 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide, 5-Ethynyl-29-deoxyuridine, wound-healing and enzyme-linked immunosorbent assays. Protein expression was analysed by Western blot. The interactions among circ_0060531, miR-330-5p and GAB1 were identified by dual-luciferase reporter or RNA immunoprecipitation assay. Circ_0060531 and GAB1 expression were significantly increased, while miR-330-5p was decreased in psoriatic skin biopsies and IL-22-stimulated HaCaT cells in comparison with controls. In function, circ_0060531 knockdown assuaged IL-22-induced cell proliferation, cell migration and inflammation. Besides, circ_0060531 acted as a miR-330-5p sponge, and regulated the processes of IL-22-treated HaCaT cells by binding to the miRNA. Under the treatment of IL-22, miR-330-5p mediated HaCaT cell damage by targeting GAB1. Importantly, circ_0060531 modulated GAB1 production by interacting with miR-330-5p. Circ_0060531 knockdown assuaged IL-22-induced keratinocyte dysfunction through miR-330-5p/GAB1 pathway, proving a novel target for the therapy of psoriasis. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 08916934
- Volume :
- 55
- Issue :
- 4
- Database :
- Academic Search Index
- Journal :
- Autoimmunity
- Publication Type :
- Academic Journal
- Accession number :
- 157269383
- Full Text :
- https://doi.org/10.1080/08916934.2022.2037127