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New & Now: Spring 2009

New View of ALS

Strong Start

God and Coal

Plastics Plant

Joint Genetics

Incentives Support

Joint Genetics

MU Protein Researchers Take Aim at Arthritis

Each year millions of Americans spend billions of dollars seeking relief from osteoarthritis, a chronic condition characterized by breakdown of cartilage in joints. Yet these mountains of prescription and over-the-counter analgesics, while effective at mitigating pain, do little to address the cause of the arthritic discomfort.

Bimal K. Ray, a professor of veterinary pathobiology at MU, is working to do something about that. “We are looking to intervene in specific molecular events to prevent the depletion of cartilage in arthritis,” Ray says.

Such an intervention, he continues, involves learning how specific protein functions are altered when inflammation is triggered, leading to pain. In a new study, recently published in the Journal of Biological Chemistry, Ray examined the interaction between two particularly promising proteins, AP-1 and SAF-1. He found that interaction between them does appear to play a significant role in inducing inflammation: specifically, the SAF-1 and AP-1 partner together to induce activation of a third gene, MMP-1. When MMP-1 is activated, collagens break down, cartilage starts to erode, and patients experience pain.

After it became clear that AP-1 and SAF-1 played a role in MMP-1 function, Ray and his team decided to explore the interaction site as a possible contact point for “competitive inhibition,” the process by which molecules bind with an enzyme or protein to decrease its activity or disable its function. Many successful pharmaceuticals rely on enzyme inhibitors. In Ray’s study, researchers identified an active site in the SAF-1 protein molecule that is involved in the interaction with AP-1 to induce the expression of the MMP-1 gene.

We looked at how and why MMP-1 is activated, particularly in the disease condition,” Ray says. “Once we understand how this gene is activated, we can design drugs to control pathways to reduce the severity of MMP-1-mediated cartilage destruction. We found strong evidence that by blocking SAF-1, MMP-1 expression is inhibited. Now, we will continue to explore the interacting domain of SAF-1 as a possible contact point for competitive inhibition.”

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Published by the Office of Research.

©2009 Curators of the University of Missouri. Click here to contact the editor.

 

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