Active exercise promotes Achilles tendon healing and is accompanied by the upregulation of collapsin response mediator protein‑2 in rats.

Abstract

Collapsin response mediator protein-2 (CRMP-2) is involved in neurite elongation and regeneration; however, its role in wound healing remains to be elucidated. The present study aimed to investigate the effects of active mobilization treatment on Achilles tendon healing and to determine the role of CRMP‑2 in the healing process. Sprague Dawley rats were subjected to Achilles tendon injury, which was verified by hematoxylin and eosin staining and scanning electronic microscopy. Immobilization induced the disruption of collagen fibril arrangement and promoted collagen fibril damage. The average collagen fibril perimeter in the active mobilization group was significantly increased compared with in the immobilization group (125.6±0.8nm vs. 119.9±1.7 nm; P<0.05). In addition, immunohistological analysis revealed that CRMP‑2 expression was significantly upregulated, particularly in the ruptured site of Achilles tendon tissues derived from animals in the mobilization group compared with the immobilization group (0.32±0.00 vs. 0.08±0.00; P<0.05). The increased CRMP‑2 levels were also confirmed by western blotting (active mobilization group, 0.71±0.03; immobilization group, 0.49±0.01 nm; P<0.05). These results indicated that active mobilization may promote Achilles tendon healing via upregulation of CRMP‑2 protein expression.