Cyclic Tensile Stretch Load and Oxidized Low Density Lipoprotein Synergistically Induce Lectin-Like Oxidized LDL Receptor-1 in Cultured Bovine Chondrocytes, Resulting in Decreased Cell Viability and Proteoglycan Synthesis

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Mechanical stimulation is known to be an essential factor in the regulation of cartilage metabolism. We tested the hypothesis that expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) can be modulated by cyclic tensile stretch load in chondrocytes. Cyclic loading of repeated stretch stress at 10 cycles per minute with 10 kPa of stress for 6 h induced expression of LOX-1 to 2.6 times control in cultured bovine articular chondrocytes, equivalent to the addition of 10 μg/mL oxidized low density lipoprotein (ox-LDL) (2.4 times control). Application of the cyclic load to the chondrocytes along with 10 μg/mL ox-LDL resulted in synergistically increased LOX-1 expression to 6.3 times control. Individual application of cyclic loading and 10 μg/mL ox-LDL significantly suppressed chondrocytes viability (84.6%±3.4% and 80.9%±3.2% of control at 24 h, respectively; n=3; p<0.05) and proteoglycan synthesis [81.0%±7.1% and 85.7%±5.2% of control at 24 h, respectively; p<0.05 when compared with 94.6%±4.6% for native-LDL (n=3)]. Cyclic loading and 10 μg/mL ox-LDL synergistically affected cell viability and proteoglycan synthesis, which were significantly suppressed to 45.6%±4.9% and 48.7%±6.7% of control at 24 h, respectively (n=3; p<0.01 when compared with individual application of cyclic loading or 10 μg/mL ox-LDL). In this study, we demonstrated synergistic effects of cyclic tensile stretch load and ox-LDL on cell viability and proteoglycan synthesis in chondrocytes, which may be mediated through enhanced expression of LOX-1 and which has important implications in the progression of cartilage degeneration in osteoarthritis.

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