Professor Vic Duance
Vic Duance is professor of biochemistry at the University of Cardiff and director of the new Arthritis Research UK Biomechanics and Bioengineering Centre.
What does your work involve?
Cartilage, a tough but flexible tissue, helps the ends of our bones to glide smoothly over each other during movement of the joints, and acts as a ‘shock-absorber’, protecting the joint from damage during normal daily life. Collagen molecules are important to the form and function of healthy joint cartilage, and damage to these molecules contributes to the failure of cartilage in arthritic disease. A large part of my research career has been devoted to understanding the structure and function of the collagens in cartilage, muscle and the intevertebral discs; tough tissues that cushion the bones of the spine. In particular, my research group has been investigating how collagens change with age and disease, and how they may also be involved in the repair of damaged cartilage.
In recent years, our research emphasis has shifted from collagen itself to the activities of the cells that make collagen (and other molecules that form cartilage). We're interested in how the complex series of molecular events that occurs in the cells in response to mechanical loading during movement of the joint may sometimes lead to damage of these molecules, and degeneration of cartilage. Using this knowledge, our ultimate aim is to devise strategies for enhancing cartilage repair in arthritis.
How long has Arthritis Research UK been funding you?
Since 1975, I think I've had continuous Arthritis Research UK support for my research, culminating in the recent award of a £2.5 million grant to establish the Arthritis Research UK Biomechanics and Bioengieering Centre here in Cardiff.
What’s the most important thing you've found out in the past 12 months? Why?
We've made significant progress in two areas. We've investigated the cytoskeleton, a kind of internal framework that gives the cartilage cell shape and structure, as well as acting as a ‘telegraph line’ through which the cell detects and responds to mechanical loading when the joint is under pressure. We've found that vimentin, one of the proteins that forms the cytoskeleton, differs significantly between osteoarthritic and normal cartilage, and that this difference may influence the way that that the ‘telegraph line’ responds to loading in osteoarthritic cartilage. Understanding this complex process will help us to tease apart the relationship between mechanical loading, cartilage damage and the development of osteoarthritis.
We've also been active in the area of tissue engineering. Repairing damaged cartilage by implanting new, healthy cartilage cells from the patient’s own body is showing some success. Prior to the repair, some of the damaged cartilage is first removed; this process causes death of some of the cells at the removal site, and we believe that this hinders successful repair. We've shown that inhibiting cell death enhances cartilage repair; this treatment may improve the success rate of cell implantation procedures.
What do you hope or expect to achieve as a result of your Arthritis Research UK funding?
A better understanding of the biological processes that lead to the development of osteoarthritis, which will enable the development of better/new targeted drugs and/or treatments. At present we have very limited interventions at our disposal to treat patients. This will be a major drive of the new centre.
What do you do in a typical day?
It'd be very nice to say that I go into the lab and set up experiments on a regular basis; unfortunately those days are long gone. I'm director of postgraduate research for the School of Biosciences. I also have a teaching commitment involving lectures generally related to my expertise in connective tissue biology.
What is your greatest research achievement?
Work over many years from my labs (Bristol and Cardiff) has made a significant contribution to our understanding of the structure and function of cartilage collagens.
Why did you choose to do this work?
After my PhD in enzyme kinetics I had a number of options but the opportunity to investigate the role of collagens in arthritis was my choice which I've never regretted.
Do you ever think about how your work can help people with arthritis?
It's easy to forget the overriding purpose when undertaking basic research as you rarely come into contact with patients. I've always had close association with clinical colleagues so I don’t believe I have ever lost sight of 'why am I doing this'. How our research can help patients was a major consideration in our bid for the Centre of Excellence for Biomechanics and Bioengineering, which is an association of basic scientists from a wide range of disciplines in collaboration with our clinical colleagues from rheumatology, orthopaedics and physiotherapy with both short and long-term goals to help sufferers of arthritis.
What would you do if you weren’t a scientist?
Biology was always my main interest in school and I find it difficult to think what else I'd want to do. Dreams of course were (and still are) to be a footballer playing for Manchester United.
Sport has always played a major part of my life: football, squash and running. Football watching (season ticket holder at Old Trafford) limits active participation as much these days, that’s my excuse. I've run six marathons and collected sponsorship for Arthritis Research UK on several occasions. However, I don’t think I could ever run enough marathons to repay my debt to Arthritis Research UK.
This article first appeard in Arthritis Today Spring 2009, issue 144.