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Osteoarthritis (OA) results from the progressive degeneration of articular cartilage.
Although multiple factors have been identified that contribute to the disease onset,
the primary risk factor is aging.
In the present study, we have proposed a novel pathway that may explain the
mechanism by which age contributes to the progression of OA.
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Total AGE in human articular cartilage.
Total AGE staining was intense in cells (arrow) and in the ECM (arrowheads).
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Advanced Glycation End products (AGEs) are products of the glycation reaction between reducing
sugars and proteins. AGEs accumulate with age in various tissues including cartilage. They affect
biochemical and biomechanical properties of the cartilage and stimulate the release of an
inflammatory chemical, TNF-α from cartilage cells.
We believe that TNF-α increases cell-cell communication through proteins known as connexins
(Cx), especially Cx43. Cx43 in turn spreads the inflammatory response and inhibits collagen
synthesis by cartilage cells. The effects of AGEs are thought to be mediated via its
receptors (AGERs).
We are currently studying the role of AGEs, putative AGE receptors and connexin-mediated
inflammatory responses using human OA cartilage tissue and a mouse chondrocyte cell line.
People involved:
Dr Shamin Shaikh (PI)
Dr Sue McGlashan (PI)
Mr Benedict Uy
Clinical collaborator:
Mr Anthony Hardy
Funded by:
The
University of Auckland Faulty of Medical and Health Sciences Faculty Development Research Fund
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