SCIENTISTS are investigating a new therapy for the treatment of tendon injuries such as tennis elbow and Achilles tendinitis after gaining new insight into the condition.
Tendon injuries are common, accounting for 30-50 per cent of all sporting injuries, and are usually caused by repetitive strain or major trauma.
While many people recover after a period of rest, a significant number of people do not because the structure of the tendon itself has permanently weakened.
A number of high-profile footballers and athletes have suffered potentially career-ending tendon injuries, including the the tennis ace Rafael Nadal who has suffered several bouts of knee tendinitis and was out of action for most of 2012 after tearing his patellar - knee - tendon.
Former Celtic goalkeeper Fraser Forster, who now plays for Southampton, has been ruled out for the rest of the season after falling awkwardly during a game in March and causing damage to his left patellar tendon, while a similar tendon injury to his right knee almost ended Scotland and Rangers goalkeeper Craig Gordon's career.
The Achilles tendon is also notoriously vulnerable among sports stars, with an Achilles tendon injury ending Belgian striker Christian Benteke's hopes of playing for his country in the 2014 World Cup.
However, researchers at Glasgow University are now trialling a new trademarked therapy, known as TenoMiR, which encourages the body to repair more effectively from tendon injuries.
Healthy tendons, connecting muscles to bones, are primarily composed of type-1 collagen, a very strong material. When injured the body responds by producing the inferior type-3 collagen to quickly repair the damage.
Normally, over time, type 3 is replaced by the stronger type-1. However, in some people, repetitive damage means the body never replaces the weaker type-3 collagen, leaving them with inherently weaker tendons and long-term symptoms, such as pain and reduced mobility.
The Glasgow trial will use injections of microRNA - small molecules that help regulate gene expression - into the tendon to drive down the production of type 3 collagen and switch to type-1 instead.
The team have already been successful in making the switch in cultured cells in the lab and in mice. They will now work with international collaborators to trial the treatment on horses, which also frequently suffer tendon injuries, particularly in racing.
Following this trial, the team intends to commercialise the treatments through a spin-out company called Causeway Therapeutics focussing on bringing safe and effective medicines to human and veterinary markets.
Neal Millar, an academic consultant orthopaedic surgeon and clinical senior research fellow at Glasgow University, said: "Tendinopathy is essentially the result of an imbalance between collagen type-1 and type-3 and we have discovered the molecular cause.
"This breakthrough has allowed us to find a way to alter the levels of collagen type-3 in tendons, with the ultimate aim to get patients with tendon injuries better quicker."
Co-investigator and senior molecular biologist Dr Derek Gilchrist added: "Our studies have revealed the previously unrecognised ability of a single microRNA to cross-regulate important functions in the early biological processes that lead to tissue repair."
Results of the previous studies by the team are published in the journal Nature Communications.
It includes a study led by Professor Iain McInnes, Director of the Institute of Infection, Immunity and Inflammation, which reveals the role of the microRNA 29a in tendon tissue repair.
The scientists found that a single microRNA - miR-29a - through its interaction with a protein, interleukin 33, plays a key role in regulating the production of collagens in tendon disease.
Loss of miR29a from human tendons results in an increase in collagen type-3 production - a key feature of tendon disease. Replacement of miR-29a in damaged tendon cells in the laboratory restores collagen production to pre injury levels.
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