Preventing Cell Death In Osteoarthritis
UK scientists have found a naturally occurring molecule in the body which may have important consequences for treating osteoarthritis
UK scientists have found a naturally occurring molecule in the body which may have important consequences for treating osteoarthritis. Researchers from The University of Manchester and the University of Westminster have found that the molecule, known as Urocortin, protects cells in the joints from being destroyed.
The discovery could help lead to the development of new medicines to prevent joint degradation — a condition which affects millions of people in the UK each year.
Osteoarthritis, a painful condition associated with a loss of joint mobility particularly in the knees, hips, hands and vertebrae, is caused by the destruction and loss of cartilage within these joints and is on the rise as people live longer.
Specialized cells called chondrocytes are responsible for producing and maintaining healthy cartilage but in osteoarthritis the number of active cells is reduced.
Professor Paul Townsend, joint lead researcher along with Dr Ian Locke, the University of Westminster, in the study published in the journal Cell Death and Disease today (11 July), said: “In osteoarthritis many different programmed cell-death chemicals are produced which cause chondrocytes to die. Our research shows that the naturally occurring molecule, Urocortin, produced by the body is essential for these chondrocyte cells to survive.”
Dr Ian Locke, director of Postgraduate Studies at the School of Life Sciences at the University of Westminster, said: “We now need to look in more detail at how Urocortin helps cells to survive in order to develop new medicines to prevent joint degradation.
“Discovering a role for this naturally occurring molecule in joint physiology opens up exciting new avenues of research towards the cause, prevention and, eventually, treatment of osteoarthritis”
The researchers found that removing Urocortin caused large numbers of the chondrocyte cells to die. However adding it protected chondrocyte cells from programmed cell-death induced by chemicals present in osteoarthritic cartilage.
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