Platelet-rich plasma-derived exosomes promote chondrocyte proliferation and inhibit apoptosis

Objective To investigate the protective effect and molecular mechanism of platelet rich plasma (PRP)-derived exosome (PRP-Exo) on interleukin-1β (IL-1β) treated chondrocytes in vitro. Methods PRP-Exo was isolated and purified, and then identified and characterized. Rat chondrocytes were treated with IL-1β to simulate in vitro osteoarthritis (OA) chondrocytes (an IL-1β group). Furthermore, the cells were also exposed to IL-1β and PRP-Exo (an IL-1β+PRP-Exo group) or activated PRP (PRP-As) (an IL-1β+PRP-Exo group). Then, cell proliferation was detected by CCK-8 assay, while apoptosis was detected by flow cytometry. Western blot and qRT-PCR were used to analyze the underlying mechanism of Furin-mediated ALK1/ALK5 signaling balance. Results Exosomes were successfully isolated and purified from PRP. The IL-1β+PRP-As and IL-1β+PRP-Exo groups showed decreases in the level of tumor necrosis factor-α (TNF-α) and cell apoptosis rate, and increases in cell proliferation rate and Furin level, compared with the IL-1β group (P<0.05). Moreover, the IL-1β+ PRP-Exo group presented better effects than the IL-1β+ PRP-As group (P<0.05). Treatment with Furin in chondrocytes significantly decreased the ratio of ALK1/ALK5 (P<0.05). IL-1β not only decreased the level of Furin in chondrocytes, but also increased the ratio of ALK1/ALK5 (P<0.05). In contrast, exposure to PRP-Exo resulted in decreases in the ratio of ALK1/ALK5 through increasing the level of Furin (P<0.05). Conclusions PRP-Exo can promote chondrocyte proliferation and inhibit apoptosis through maintaining Furin-mediated ALK1/ALK5 balance.