Glasgow: 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 (tendinopathies) are common, accounting for 30-50% 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. 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. This type of collagen is not as strong as type-1 and is more
prone to damage. Normally, over time, type 3 is replaced by the stronger
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.
Scientists at the University of Glasgow are trialling a new therapy
(TenoMiR™) for treating tendinopathy after being awarded a High Growth
Spinout grant from Scottish Enterprise.
The trial will use injections of microRNA – small molecules that help
regulate gene expression – into the tendon to ‘dial-down’ the
production of type 3 collagen and switch to type-1.
The Glasgow 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
Neal Millar, an academic consultant orthopaedic surgeon and clinical
senior research fellow at the University of Glasgow, 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
Co–investigator and senior molecular biologist Dr Derek Gilchrist
commented that: “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, which also includes
Professor Iain McInnes, Director of the Institute of Infection, Immunity
and Inflammation within the University are published in Nature
Communications and reveal the role of the microRNA 29a in tendon tissue
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. The research was supported by the Scottish Funding
Council, Wellcome Trust and the Academy of Medical Sciences.