p53 in rheumatoid arthritis: friend or foe?

Abstract

The knowledge of transcription factors and proto-oncogenes has influenced the understanding of cell regulation, cell cycle, and apoptotic cell death in rheumatoid arthritis (RA) synovium. In addition, the development of normal synovial fibroblasts into transformed-appearing aggressive synovial fibroblasts may be triggered by the lack of antiproliferative factors, such as p53, p53-associated molecules, other tumor suppressors, as well as by upregulation of anti-apoptotic genes. Therefore, data derived from experiments such as those performed by Tak and colleagues in this issue of Arthritis Research not only enrich the intensive discussion addressing the impact of p53 on RA pathophysiology, they also may facilitate development of novel therapeutic approaches including p53-targeted gene therapy.

Figure 1

Upregulation of MDM2-like p53 binding protein (arrow) following adenovirus-based TNFaRp55 gene transfer into rheumatoid synovial fibroblasts. (Analysis performed by Elena Neumann, University of Regensburg, Germany, using a Clontech Atlas® DNA array system. TNFaRp55 Ad5 generously provided by Dr John Mountz, University of Birmingham, AL, USA.)