Blood-clotting protein plays key role in development of inflammatory diseases

November 17th, 2007 - 1:24 pm ICT by admin  

Washington, Nov 17 (ANI): A new research, conducted by Cincinnati Children’s Hospital Medical Center has revealed that fibrin, a protein normally involved in blood clotting, plays a key role in the inflammatory response and development of rheumatoid arthritis.

The study, led by Jay Degen, Ph.D., a researcher in Developmental Biology at Cincinnati Childrens, has suggested that the therapies designed to interrupt the localized interaction of inflammatory cells and fibrin may help arthritis patients.

Our study establishes that fibrin is a powerful, although context-dependent, determinant of inflammatory joint disease, said Degen.

These findings also suggest that pharmacologically interrupting the interaction of fibrin and aMB2 might be efficacious in the treatment of arthritic disease as well as many other inflammatory diseases, such as multiple sclerosis, he added.

Rheumatoid arthritis is a painful and debilitating disease involving chronic inflammation, tissue degeneration, loss of cartilage and bone and ultimately loss of joint mobility and function, according to the National Institute of Arthritis and Musculoskeletal and Skin Diseases.

According to researchers, although the diseases precise cause is not fully known, activation of specific components in the bodys immune system seem to play a major role in its onset and early progression.

Fibrin deposits are a prominent feature of arthritic joints and the protein appears to be a link between systems that control inflammation and bleeding within joints.

Dr. Degen and his colleagues explained that in arthritic joints, the mesh-like matrices formed by fibrin to create blood clots may control local activity of inflammatory cells as well as support inappropriate tissue reorganization.

For the study, researchers used genetically engineered mice with collagen-induced arthritis of the knee and paw.

The mice were designed to have selective alterations in the production of fibrinogen, a precursor to fibrin, to allow researchers to evaluate the inflammatory impact of fibrin, especially as it interacts with aMB2.

The study is published in the November issue of The Journal of Clinical Investigation. (ANI)

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