LAUSR

Mimecan, or osteoglycin, belongs to the family of small leucine-rich proteoglycans. In connective tissues mimecan is implicated in the development and maintenance of normal collagen fibrillar organization. Since collagen fibrils are responsible for tissue reinforcement, the absence of mimecan could lead to abnormal tissue mechanical properties. Here, we carried out a preliminary investigation of possible changes in the mechanical properties of tendons in mice lacking a functional mimecan gene, as a function of age. Tail tendons were dissected from mimecan gene knockout (KO) and wild type (WT) mice at ages 1, 4 and 8 months and mechanical properties evaluated using a microtensile testing equipment. Mimecan gene knockout resulted in changes in tendon elasticity- and fracture-related properties. While tendons of WT mice exhibited enhanced mechanical properties with increasing age, this trend was notably attenuated in mimecan KO tendons, with the exception of fracture strain. When genotype and age were considered as cross factors, the diminution in the mechanical properties of mimecan KO tendons was significant for yield strength, modulus and fracture strength. This effect appeared to affect the mice at 4 month old. These preliminary results suggest that mimecan may have a role in regulating age-dependent mechanical function in mouse tail tendon.