UAMS, Harvard Researchers Make Arthritis Breakthrough

By Nate Hinkel

 Jerry Ware works at a platelet aggregometer, a device that measures how well a person’s platelets are functioning.

June 11, 2010| A breakthrough in research on blood platelets has the potential to bring new treatments for those with rheumatoid arthritis, said a UAMS scientist who assisted in the project.

A recently published arthritis study co-authored by UAMS’ Jerry Ware, Ph.D., has been recognized by the Arthritis Foundation as the top advance in arthritis research for the past year.

Ware, professor of physiology and biophysics at the University of Arkansas for Medical Sciences (UAMS), collaborated with Harvard Medical School’s David Lee, Ph.D., on the study and article, “Platelets Amplify Inflammation in Arthritis Via Collagen-Dependent Microparticle Production.” It was published in the January 2010 issue of Science.

Their work revealed that blood platelets can enter joints affected by rheumatoid arthritis (RA) and form microparticles that promote inflammation in the joints.

“The relevance of this finding for future treatment of RA (rheumatoid arthritis) is substantial,” the Arthritis Foundation states in its Research Update. “It shows a new way by which blood platelets impact inflammation, helps explain why some newer medications are sometimes not effective in treating RA, and opens up a new target for drug development.”

Ware said the serendipitous discovery began a few years ago with a phone call from Lee, who was experimenting with synovial fluid from patients with RA. Lee e-mailed photos to Ware, who noticed the strong platelet signaling as a result of Lee’s staining with a platelet-specific protein. But Ware also recognized that the “platelets” they were seeing might actually be platelet fragments called microparticles that had found their way into the joints.

As Lee’s study progressed, Ware, by happenstance, was able to provide mice that were exactly of the type needed for advancing their work. The mice were bred so that each was missing a collagen receptor on the surface of their platelets. And that collagen receptor turned out to be the receptor that was worsening the inflammatory disease in patients with rheumatoid arthritis.

“I didn’t make the mice for that reason at all,” Ware said. “Originally they were made to study the role of collagen in normal clot formation.”

Ware agrees with the Arthritis Foundation’s assessment that the study’s findings could lead to new treatments for RA patients. The research was taken to UAMS BioVentures, and a UAMS and Harvard patent is pending. BioVentures was created in 1997 to help UAMS researchers patent their discoveries, license intellectual property and assist with start-up companies.

Ware is excited about the discovery because of its potential benefit to RA patients. He said he’s also happy because it shows platelet research has matured beyond clotting.

“Platelet scientists are no longer just coagulation experts,” Ware said. “We’re also starting to learn about cancer, immunology and inflammation, so that excites me too. I get to learn some new things.”