Synovial Fibroblasts (SFs) are unique mesenchymal cells populating the synovium, a membrane that defines diarthroses. Under normal conditions, SFs assure the structural and dynamic integrity of synovial joints by coordinating the composition of the synovial fluid and the extracellular matrix of the joint lining. In rheumatoid arthritis (RA) however, SFs revert themselves from a homeostatic regulator to a pathogenic orchestrator of the degenerative joint disease by increasing in number and controlling the destructive pannus that characterizes synovia of patients with RA. Whether the excess of SFs in pannus originates mostly from a discrepancy in their physiological regenerative capacity or an increased differentiation and migration of mesenchymal stem cells could also contribute, still remains obscure. RA SFs are resistant to apoptosis in vitro, suggesting that abnormalities persist even upon their removal from the cytokine and growth factor milieu of the RA synovium.  

The emerging evidence on the signaling mechanisms controlling death indicates that the dissection of the molecular interplay between cell death and survival/inflammation could significantly contribute to our understanding of the processes involved in development, homeostasis, inflammatory and degenerative pathologies. Thus, using cell-targeted genetic methodologies, cell-tracing techniques and animal disease modeling we aim to improve our understanding for the physiological significance of SFs as well as their cell-specific role in disease. A better insight in the details of the general processes involved will likely allow the development of more targeted and effective drugs.

 

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