Exosomes from human umbilical cord mesenchymal stem cells inhibit ROS production and cell apoptosis in human articular chondrocytes via the miR‐100‐5p/NOX4 axis

Cyclic strain‐induced chondrocyte damage is actively involved in the pathogenesis of osteoarthritis and arthritis. MicroRNAs (miRNAs) carried by exosomes have been implicated in various diseases. However, the role of miR‐100‐5p in cyclic strain‐induced chondrocyte damage remains to be elucidated. miR‐100‐5p and NADPH oxidase 4 (NOX4) were silenced or overexpressed in human primary articular chondrocytes. PKH‐67 Dye was used to trace exosome endocytosis. Reactive oxygen species (ROS) production was monitored using DCFH‐DA. Cell apoptosis was measured using a flow cytometer. Quantitative RT‐PCR and Western blots were used to evaluate gene expression. Cyclic strain promoted ROS production and apoptosis in primary articular chondrocytes in a time‐dependent manner. HucMSCs‐derived exosomal miR‐100‐5p inhibited cyclic strain‐induced ROS production and apoptosis in primary articular chondrocytes. miR‐100‐5p directly targeted NOX4. Overexpressing NOX4 attenuated hucMSCs‐derived exosomes‐mediated protective effects in primary articular chondrocytes. Cyclic strain promotes ROS production and apoptosis in primary articular chondrocytes, which was abolished by hucMSCs‐derived exosomal miR‐100‐5p through its target NOX4. The findings highlight the importance of miR‐100‐5p/NOX4 axis in primary articular chondrocytes injury and provide new insights into therapeutic strategies for articular chondrocytes injury and osteoarthritis.