Knockdown of DAPK1 attenuates IL-1ß-induced extracellular matrix degradation and inflammatory response in osteoarthritis chondrocytes via regulating the p38 MAPK-signaling pathway.
Allergol Immunopathol (Madr)
; 50(6): 169-175, 2022.
Article
en En
| MEDLINE
| ID: mdl-36335461
ABSTRACT
OBJECTIVE:
To reveal the possible effects of death-associated protein kinase 1 (DAPK1) on the progression of osteoarthritis (OA) and the potential underlying mechanism.METHODS:
The expression of DAPK1 in OA and normal samples and interleukin (IL)-1ß-stimulated chondrocytes was analyzed by quantitative real-time polymerase chain reaction and Immunoblot assay. Cell viability, proliferation, and apoptosis in DAPK1-knockdown cells stimulated with IL-1ß were detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) solution, 5-ethynyl-2ß-deoxyuridine staining and flow cytometry. The chondrocyte degradation and inflammatory response in IL-1ß-induced chondrocytes were investigated by Immunoblot analysis and enzyme-linked-immunosorbent serologic assay. In addition, the effect of DAPK1 on p38 mitogen-activated protein kinase (MAPK) activation was analyzed by immunoblot assay.RESULTS:
This study revealed that DAPK1 was highly expressed in OA patients and IL-1ß-induced chondrocytes. Down-regulation of DAPK1 enhanced IL-1ß-induced chondrocyte proliferation. DAPK1 knockdown inhibited IL-1ß-induced chondrocyte degradation. In addition, DAPK1 depletion inhibited IL-1ß-induced chondrocyte inflammation. Mechanically, it was revealed that down--regulation of DAPK1 could inhibit the p38 MAPK pathway, and therefore affected progression of OA.CONCLUSION:
DAPK1 knockdown attenuates IL-1ß-induced extracellular matrix degradation and inflammatory response in OA chondrocytes by regulating the p38 MAPK pathway.Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Osteoartritis
/
MicroARNs
Límite:
Humans
Idioma:
En
Revista:
Allergol Immunopathol (Madr)
Año:
2022
Tipo del documento:
Article
País de afiliación:
China