Platelet-released growth factors protect articular chondrocytes from inflammatory condition

Although platelet-released growth factors (PRGF) can protect cells from inflammation or oxidative stress condition, their therapeutic efficacy for articular cartilage degeneration has been little discussed. The purpose of this study was to investigate the effect of PRGF on human articular chondrocytes under inflammatory conditions.

Human C-28/I2 chondrocytes were treated with PRGF, the production from liquid-preserved platelet concentrates obtained by platelet apheresis from human volunteers. Cell proliferation/viability, and collagen type (COL) II and SOX9 gene expressions for chondrogenesis were evaluated with different PRGF concentrations. Additionally, in vitro inflammatory condition was mimicked by stimulating the cells with tumor necrosis factor (TNF)-α. Under inflammation, cell viability, TNF-α gene expression, and the protein levels of cytokines including TNF-α, interleukin (IL)-1β and -6, and vascular endothelial growth factor (VEGF) angiogenesis marker, were compared with and without PRGF treatment.

Cell proliferation/viability, and SOX9 and COL II expressions in chondrocytes stimulated with 10% PRGF were significantly higher than without treatment. Cell viability with 10% PRGF was also statistically higher than without treatment under inflammation. The TNF-α gene expression with 10% PRGF was significantly lower than without treatment under inflammation. The protein levels of endogenous TNF-α with 5% PRGF, IL-1β with 10% PRGF, and IL-6 with 5 and 10% PRGF in chondrocytes were significantly lower than untreated ones under inflammation. The VEGF-protein level in chondrocytes stimulated with 20% PRGF was significantly higher than without treatment under inflammation, while there was no significant difference between with 10% PRGF and without treatment.

Our results reveal that optimal PRGF treatment leads to the increase of chondrocyte proliferation/viability and chondrogenic markers, while it increased cell viability but reduced IL-1β and IL-6 expressions under inflammatory condition, suggesting the therapeutic role of PRGF for protection from articular cartilage degeneration through anti-inflammatory effects.