Hypoxia inducible factor-2 alpha (HIF-2α) overexpression effect on primary mouse articular chondrocytes. Hypoxia inducible factor-2 alpha (HIF-2α) overexpression effect on primary mouse articular chondrocytes

Gene expression profiling of primary mouse articular chondrocyte infected with recombinant adenovirus expressing the hypoxia inducible factor-2 alpha (HIF-2α) protein. In this study, we have attempted to explore the effects of HIF-2α overexpression on mouse transcriptome and have identified numerous genes which are involved in osteoarthritis pathogenesis. Overall design: Primary mouse articular chondrocytes were isolated from mouse femoral condyles and tibial plateaus cartilage tissue (WT ICR 5-day-old mice) and were infected with null (control) or recombinant adenovirus expressing hypoxia inducible factor-2 alpha (HIF-2α, Ad-Epas1) for 24 hours. At 24 hours post-infection, total RNA was extracted from infected with null (control) adenovirus (4 biological replicates) or infected with recombinant adenovirus expressing the hypoxia inducible factor-2 alpha (4 biological replicates) on primary mouse articular chondrocytes and subjected to microarray analysis.