Effects of administration of transforming growth factor (TGF)-beta1 and anti-TGF-beta1 antibody on the mechanical properties of the stress-shielded patellar tendon.
Previous studies have shown that, in the stress-shielded patellar tendon, the mechanical properties of the tendon were dramatically reduced and TGF-beta was over-expressed in tendon fibroblasts. In the present study, therefore, we tested two supportive hypotheses using 40 rabbits: One was that an application of TGF-beta1 might significantly increase the tensile strength and the tangent modulus of the stress-shielded patellar tendon. The other one was that an administration of anti-TGF-beta1 antibody might significantly reduce the mechanical properties of the stress-shielded patellar tendon. In the results, an application of 4-ng TGF-beta1 significantly increased the tangent modulus of the stress-shielded patellar tendon at 3 weeks (p = 0.019), compared with the sham treatment. Concerning the tensile strength, the 4-ng TGF-beta1 application increased the average value, but a statistical significance was not reached. An application of 50-microg anti-TGF-beta1 antibody significantly reduced the tangent modulus and the tensile strength of the stress-shielded patellar tendon at 3 weeks (p = 0.0068 and p = 0.0355), compared with the sham treatment. Because the stress-shielding treatment used in this study dramatically reduces the tangent modulus and the tensile strength of the patellar tendon, the present study suggested that an administration of TGF-beta1 weakly but significantly inhibited the reduction of the mechanical properties of the stress-shielded patellar tendon, and that inactivation of TGF-beta1 with its antibody significantly enhanced the reduction of the mechanical properties that occurs in the stress-shielded patellar tendon. These results suggested that TGF-beta1 plays an important role in remodeling of the stress-shielded patellar tendon.
Katsura
Taro
T
Department of Sports Medicine and Joint Reconstruction Surgery, Hokkaido University School of Medicine, Kita-15 Nishi-7, Kita-ku, Sapporo, 060-8638 Japan.
Tohyama
Harukazu
H
Kondo
Eiji
E
Kitamura
Nobuto
N
Yasuda
Kazunori
K
D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D001696:Biomechanical Phenomena; D005260:Female; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism; D017847:Patellar Ligament / Q000187:drug effects* / Q000503:physiopathology; D011817:Rabbits; D012038:Regeneration / Q000187:drug effects / Q000502:physiology*; D013314:Stress, Mechanical; D013718:Tensile Strength / Q000187:drug effects; D053773:Transforming Growth Factor beta1 / Q000276:immunology / Q000494:pharmacology*
D000911:Antibodies, Monoclonal; D053773:Transforming Growth Factor beta1