GDF-5 deficiency alters stress-relaxation properties in mouse skin.

Objective: Growth / Differentiation Factor-5 (GDF-5) is a member of the family of Bone Morphogenetic Proteins (BMPs) known to have diverse effects on musculoskeletal connective tissues [1,2]. Recently, biomechanical and ultrastructural abnormalities have been demonstrated in several collagen-rich tissues from GDF-5 deficient mice, including Achilles tendon, tail tendon, and long bone [3-5]. In previous studies of mouse tail tendon, no differences were found in quasi-static mechanical behavior between GDF-5 deficient and control tendons. However, in stress-relaxation (time-dependent) tests, mutant tendon relaxed more slowly, and to a lesser extent, than did controls [5]. Ultrastructural analyses suggest that these results may be due to an increased prevalence of abnormally shaped type I collagen fibrils in the mutant tissue, thereby providing an increased fibril surface area for molecular interactions between fibrils and other extracellular matrix components. To investigate the hypothesis that GDF-5 deficiency affects the biomechanical behavior of other type I collagen-rich tissues, we compared skin from GDF-5 deficient mice with skin from control mice in quasi-static and stress-relaxation tests. In addition, collagen fibril ultrastructure was qualitatively examined with electron microscopy of skin samples from representative animals.