| The relative energy metabolism of chondrocytes in normal human adult articular cartilage has been assigned as 80% of the glucose being processed through glycolysis and only 20% of the glucose being processed through oxidative phosphorylation. This is mainly due to the avascular nature of the tissue, resulting in a decrease in the amount of oxygen supplied to chondrocytes within articular cartilage. However, ultrastructural examination of chondrocytes from articular cartilage via electron microscopy showed that these cells contain a large number of mitochondria. Chondrocytes were examined with the mitochondrial probe, JC-1 to analyze mitochondrial membrane potential as a measure of mitochondrial activity. Based on flow cytometry and confocal microscopy, chondrocytes from the superficial layer of articular cartilage contained mitochondria with higher membrane potential. Antimycin A inhibited the mitochondrial membrane potential in a dose dependent manner. There is also little direct evidence that chondrocytes in adult articular cartilage proliferate in vivo, however the organization of superficial chondrocytes in the human ankle, in chondrons consisting of 2–4 cells suggests that these cells may proliferate. Based on this and the higher mitochondrial activity in the chondrocytes from the superficial layer, we hypothesized that there is a correlation between the mitochondrial activity within chondrocytes and their ability to proliferate. Superficial chondrocytes were analyzed for two proliferation markers, proliferating cell nuclear antigen (PCNA) and Cyclin B, which are localized to the nucleus during DNA synthesis and prophase of the cell cycle. Cells in the superficial zone of articular cartilage were positive for PCNA and Cyclin B, both of which were present in the nucleus. The inhibitor Antimycin A was able to reduce the number of chondrocytes that were positive for PCNA from 23.6% to 2.8% in a dose dependent manner, suggesting that superficial zone chondrocytes have the capacity to proliferate and that energy for that proliferation may come from the mitochondria with higher membrane potential. |
