Knockdown of DAPK1 attenuates IL-1β-induced extracellular matrix degradation and inflammatory response in osteoarthritis chondrocytes via regulating the p38 MAPK-signaling pathway

• Jie Wei ^[1] ; Chen Gao ^[2] ; Ke Hu ^[3] ; Mingyue Li ^[4] ; Jingshi Li ^[2] ; Mengman Shen ^[4] ; Shuyu Zhang ^[5]
  1. [1] Changzhi Medical College

     Changzhi Medical College

     China

     
  2. [2] Department of Sports Medicine, Military Sports Training Center of the Training Management Department of the Central Military Commission, Beijing, China
  3. [3] Basketball Project Room, Military Sports Training Center of the Training Management Department of the Central Military Commission, Beijing, China.
  4. [4] Military Sports Research Office, Military Sports Training Center of the Training Management Department of the Central Military Commission, Beijing, China
  5. [5] Department of Rehabilitation, Beidahuang Group General Hospital, Beijing, China.

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• Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 50, Nº. 6, 2022, págs. 169-175
• Idioma: inglés
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• Resumen

  • 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)-1β-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-1β were detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) solution, 5-ethynyl-2β-deoxyuridine staining and flow cytometry. The chondrocyte degradation and inflammatory response in IL-1β-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-1β-induced chondrocytes. Down-regulation of DAPK1 enhanced IL-1β-induced chondrocyte proliferation. DAPK1 knockdown inhibited IL-1β-induced chondrocyte degradation. In addition, DAPK1 depletion inhibited IL-1β-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-1β-induced extracellular matrix degradation and inflammatory response in OA chondrocytes by regulating the p38 MAPK pathway.