SIRT5 reduces the inflammatory response and barrier dysfunction in IL-17A-induced epidermal keratinocytes.
Allergol Immunopathol (Madr)
; 51(1): 30-36, 2023.
Article
em En
| MEDLINE
| ID: mdl-36617819
ABSTRACT
Psoriasis is a chronic multisystemic inflammatory disease with inflammatory cell infiltration, hyperproliferation of keratinocytes in skin lesions, and epidermal barrier dysfunction. Normal human epidermal keratinocytes (NHEKs) were stimulated with interleukin 17A (IL-17A). The expression levels of sirtuin-5 (SIRT5) were analyzed by RT-qPCR and western blot assay. The proliferation levels of NHEKs were assessed by EdU staining. The expression of ELOVL1 and ELOVL4 was analyzed by RT-Qpcr, and the expression levels of filaggrin, loricrin, and aquaporin-3 were analyzed by RT-qPCR and western blot. Extracellular signal-regulated kinase 1/2 (ERK1/2) activator t-butylhydroquinone was used to activate ERK1/2. Here, we show that SIRT5 overexpression reduces cell viability and cell proliferation, and improves barrier dysfunction in IL-17A-treated human epidermal keratinocytes, this effect of which is significantly blunted by the ERK1/2 activator. In epidermal keratinocytes, SIRT5 decreases cell proliferation and inflammation and improves barrier dysfunction via ERK/STAT3. This study reveals the role of SIRT5 in the pathogenesis of psoriasis, epidermal hyperplasia, keratinocyte-mediated inflammatory responses, and barrier dysfunction, the role of which is mediated by ERK/STAT3.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Psoríase
/
Queratinócitos
/
Interleucina-17
/
Sirtuínas
Limite:
Humans
Idioma:
En
Revista:
Allergol Immunopathol (Madr)
Ano de publicação:
2023
Tipo de documento:
Article
País de afiliação:
China