Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: New insights into integrin signalling: implications for rheumatoid arthritis synovial fibroblasts. | Arthritis Research Therapy Vol 5 No 3 Pap Viewpoint New insights into integrin signalling implications for rheumatoid arthritis synovial fibroblasts Thomas Pap Division of Experimental Rheumatology University Hospital Magdeburg Germany and Center of Experimental Rheumatology Department of Rheumatology University Hospital Zurich Switzerland Corresponding author Thomas Pap e-mail Received 23 Mar 2003 Revisions requested 25 Mar 2003 Revisions received 28 Mar 2003 Accepted 28 Mar 2003 Published 10 Apr 2003 Arthritis Res Ther 2003 5 154-155 DOI ar765 2003 BioMed Central Ltd Print ISSN 1478-6354 Online ISSN 1478-6362 Introduction Fibronectin is an important component of the articular extracellular matrix ECM . Both fibronectin itself and fragments of fibronectin bind to integrin receptors on mesenchymal cells and exert a variety of effects. Of these regulation of cell growth migration and survival are most prominent. However it has also been demonstrated that injection of fibronectin fragments into joints may cause depletion of proteoglycans 1 and induce the production of matrix degrading enzymes 2 3 . Binding of fibronectin to integrin receptors results in the activation of tyrosine phosphorylation signals and it is now accepted that the focal adhesion-associated tyrosine kinase FAK plays a central role in this process. Interactions of FAK with the src family of protein tyrosine kinases Src-PTKs have been described as being crucial for the initiation of signalling cascades that ultimately mediate the effects of integrins. Despite this general concept early molecular events that regulate the association of FAK with Src-PTKs and thus link integrin signalling to cellular activation are unclear. Specifically little is known about the role of receptor protein tyrosine phosphatases PTPs which have been implicated as positive and negative regulators of integrin signalling. A recent report from Zeng and coworkers 4 sheds new light on
