TY - JOUR
T1 - Stress deprivation simultaneously induces over-expression of interleukin-1beta, tumor necrosis factor-alpha, and transforming growth factor-beta in fibroblasts and mechanical deterioration of the tissue in the patellar tendon
AU - Uchida, Hisaya
AU - Tohyama, Harukazu
AU - Nagashima, Kazuo
AU - Ohba, Yasuko
AU - Matsumoto, Hideo
AU - Toyama, Yoshiaki
AU - Yasuda, Kazunori
PY - 2005/4
Y1 - 2005/4
N2 - To test the hypothesis that stress deprivation induces over-expression of cytokines in the patellar tendon, 40 rats were divided into the following two groups. In the stress-shielded group, we slackened the patellar tendon in the right knee by drawing the patella toward the tibial tubercle with flexible wires. In the control group, we performed a sham operation on the right knee. Animals were killed at 2 or 6 weeks for immunohistological evaluation and biomechanical examination. For IL-1β, TNF-α and TGF-β, the ratio of positively stained specimens to total specimens was significantly higher in the stress-shielded tendons than in the control tendons. The elastic modulus of the stress-shielded tendon was significantly lower than that of the control tendon, while the cross-sectional area of the stress-shielded tendon was significantly greater than that of the control tendon. Therefore, the present study indicated that stress shielding induced the over-expression of IL-1β, TNF-α and TGF-β in patellar tendon fibroblasts with mechanical deterioration of the tendon. Regarding clinical relevance, the present study suggests a possible application of an anti-IL-1β or anti-TNF-α strategy for reducing the mechanical deterioration of tendons and ligaments in response to stress deprivation, although this study did not directly show that over-expression of IL-1β or TNF-α in response to stress deprivation was the causation of mechanical deterioration of tendons.
AB - To test the hypothesis that stress deprivation induces over-expression of cytokines in the patellar tendon, 40 rats were divided into the following two groups. In the stress-shielded group, we slackened the patellar tendon in the right knee by drawing the patella toward the tibial tubercle with flexible wires. In the control group, we performed a sham operation on the right knee. Animals were killed at 2 or 6 weeks for immunohistological evaluation and biomechanical examination. For IL-1β, TNF-α and TGF-β, the ratio of positively stained specimens to total specimens was significantly higher in the stress-shielded tendons than in the control tendons. The elastic modulus of the stress-shielded tendon was significantly lower than that of the control tendon, while the cross-sectional area of the stress-shielded tendon was significantly greater than that of the control tendon. Therefore, the present study indicated that stress shielding induced the over-expression of IL-1β, TNF-α and TGF-β in patellar tendon fibroblasts with mechanical deterioration of the tendon. Regarding clinical relevance, the present study suggests a possible application of an anti-IL-1β or anti-TNF-α strategy for reducing the mechanical deterioration of tendons and ligaments in response to stress deprivation, although this study did not directly show that over-expression of IL-1β or TNF-α in response to stress deprivation was the causation of mechanical deterioration of tendons.
KW - Cytokine
KW - Mechanical properties
KW - Patellar tendon
KW - Stress deprivation
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U2 - 10.1016/j.jbiomech.2004.05.009
DO - 10.1016/j.jbiomech.2004.05.009
M3 - Article
C2 - 15713300
AN - SCOPUS:13844274954
SN - 0021-9290
VL - 38
SP - 791
EP - 798
JO - Journal of Biomechanics
JF - Journal of Biomechanics
IS - 4
ER -