Adenosine A2A Receptor Null Chondrocyte Transcriptome Resembles that of Human Osteoarthiris Chodnrocytes

Osteoarthritis (OA) is a highly prevalent and morbid disease affecting over 30 million Americans. Effective drugs and treatments to halt the progression or reverse OA pathogenesis are not available, creating a need for translational research in the field. The A2AR null mouse is an important animal model for the understanding of disease pathogenesis and the development of novel therapies. We have previously shown that these mice develop OA spontaneously by age 16 weeks and that liposomal adenosine is able to reverse established OA in animal models of post-traumatic OA and overbearing/overweight OA. We here illustrate how the A2ARKO transcriptome shows early compromise of cell viability and compares to that of human OA chondrocytes. Overall design: A2ARKO and WT primary neonatal chondrocytes were isolated and submitted for RNA sequencing with subsequent KEGG pathway analysis to characterize drivers of OA. oPOSSUM and the flatiron database were used for transcription factor binding enrichment and tissue specific network analyses.