SIRT5 reduces the inflammatory response and barrier dysfunction in IL-17A-induced epidermal keratinocytes
Allergol. immunopatol
; 51(1): 30-36, ene. 2023. graf
Artículo
en Inglés
| IBECS
| ID: ibc-214019
Biblioteca responsable:
ES1.1
Ubicación: ES15.1 - BNCS
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 (AU)
Texto completo:
Disponible
Colección:
Bases de datos nacionales
/
España
Base de datos:
IBECS
Asunto principal:
Psoriasis
/
Queratinocitos
/
Interleucina-17
/
Sirtuinas
/
Células Epiteliales
Límite:
Humanos
Idioma:
Inglés
Revista:
Allergol. immunopatol
Año:
2023
Tipo del documento:
Artículo
Institución/País de afiliación:
Jinan University/China
/
Pingshan General Hospital of Southern Medical University/China
/
Southern University of Science and Technology)/China