|dc.contributor.author||Taylor, Sarah Louise||
|dc.description.abstract||Injuries of energy-storing tendons such as the equine superficial digital flexor tendon
and the human Achilles tendon are responsible for significant health and financial costs.
A good model of acute tendinopathy of energy-storing tendons is required to better
understand the changes that occur within the injured tendon and thereby to aid in the
development of successful treatment regimens. Connexin43 plays an important role in
wound healing and is involved with the spread of cell death signals following injury.
Understanding the effect of Connexin43 modulation on tendon injury could improve
tendon healing rate and quality.
Models of acute injury were developed in the pelvic limb superficial digital flexor
tendon of sheep and adapted for the thoracic limb superficial digital flexor tendon in
horses. The sheep injury model was used to investigate the effects of injury on
Connexin43 expression and the effect of Connexin43 antisense oligodeoxynucleotides
in the peracute (2 to 4 hours) post injury stage. The model in horses was monitored
clinically and ultrasonographically and these findings were related to the gross and
histological changes at post mortem after 4 days. A surgical model of acute tendon
injury was successfully developed and applied to sheep and horse energy-storing
tendons. This has potential for modelling tendon injury in horses and humans. Increased
Connexin43 levels were measured at the injury site at 2-4 hours post injury. Antisense
oligodeoxynucleotides did not significantly reduce Connexin43 levels in the injured
tendons in the acute period.
Equine superficial digital flexor tendon-derived fibroblasts derived from different
horses exhibit different cell growth rates that may be an indicator of a genetic ability to
heal more effectively.
The new models of acute tendon injury may facilitate development of an accurate model
of clinical tendon injury in energy storing tendons to improve our knowledge of the
problem and our treatments.||en
|dc.title||Novel models of tendon injury and gap junction modulation in tendon cell and tissue repair : a dissertation presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy at Massey University, Turitea, Manawatu, New Zealand||en
|thesis.degree.name||Doctor of Philosophy (Ph.D.)||en