Figure 3
From: Hypoxia. HIF-mediated articular chondrocyte function: prospects for cartilage repair
Hydroxylase inhibition, like hypoxia, upregulates SOX9 in human articular chondrocytes by an HIF-2α dependent mechanism. (a) The non-specific hydroxylase inhibitor dimethyloxaloylglycine (DMOG) upregulates hypoxia-inducible factor (HIF)-1α, HIF-2α, and SOX9 transcription factors in human articular chondrocytes. (b) Like hypoxia, DMOG induction of SOX9 in human articular chondrocytes is HIF-2α, but not HIF-1α, dependent. Luc, luciferase; siRNA, small interfering RNA. (c) Relative mRNA levels of HIF-targeting prolyl hydroxylase domain (PHD) enzymes in human articular chondrocytes (from n = 7 patients) exposed to both hypoxia and normoxia. ***P < 0.001. Error bars indicate standard deviation about the mean.