RIP2 knockdown inhibits cartilage degradation and oxidative stress in IL-1β-treated chondrocytes via regulating TRAF3 and inhibiting p38 MAPK pathway
Copyright © 2021. Published by Elsevier Inc.
| Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 232(2021) vom: 01. Nov., Seite 108868 |
|---|---|
| 1. Verfasser: | |
| Weitere Verfasser: | , , , , |
| Format: | Online-Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2021
|
| Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
| Schlagworte: | Journal Article Research Support, Non-U.S. Gov't Osteoarthritis RIP2 TRAF3 p38 IL1B protein, human Interleukin-1beta TNF Receptor-Associated Factor 3 TRAF3 protein, human mehr... |
| Zusammenfassung: | Copyright © 2021. Published by Elsevier Inc. Receptor-interacting protein 2 (RIP2) is a key mediator implicated in multiple cellular processes, and its dysregulation has been recently reported in colitis, asthma and other inflammatory diseases. However, the effects of RIP2 on osteoarthritis (OA) and the underlying mechanisms remain unclear. In this study, we found that RIP2 expression was upregulated in human articular cartilage tissues with OA and interleukin-1β (IL-1β)-treated chondrocytes. Knockdown of RIP2 inhibited IL-1β-induced extracellular matrix (ECM) and oxidative stress. Moreover, knockdown of TRAF3 reversed the effects of RIP2 silencing on cartilage degradation and oxidative stress in IL-1β-induced chondrocytes. In addition, p38 mitogen-activated protein kinase (MAPK) activator dehydrocorydalmine chloride (Dc) also reversed the effects of RIP2 silencing on IL-1β-induced chondrocytes. Taken together, our data reveal that RIP2 knockdown inhibits cartilage degradation and oxidative stress in IL-1β-treated chondrocytes by regulating TRAF3 expression and p38 MAPK pathway activation |
|---|---|
| Beschreibung: | Date Completed 26.11.2021 Date Revised 26.11.2021 published: Print-Electronic Citation Status MEDLINE |
| ISSN: | 1521-7035 |
| DOI: | 10.1016/j.clim.2021.108868 |