Joint
contracture is a fibroproliferative disorder that restricts joint mobility, resulting in tissue degeneration and
deformity. However, the etiology of joint
contracture is still unknown.
Chaperonin containing T-complex polypeptide subunit eta (CCT-eta) is reported to increase in fibrotic diseases. The purpose of this study was to investigate whether CCT-eta is implicated in joint
contracture and to determine the role of CCT-eta in the progression of joint
contracture by analyzing a rat model. We immobilized the left knee joint of rat by internal fixation for 8 weeks. The non-immobilized right leg served as a control. The range of motion (ROM) of the knee was investigated. Fibroblasts were obtained from the posterior joint capsule of the joints. The outcome was followed by quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, fibroblast migration assay, and
collagen assay. The effect of CCT-eta on the functions of fibroblasts was observed by utilizing a short inhibitory
RNA (
siRNA) targeting CCT-eta. The ROM of the immobilized joints was significantly limited compared to the contralateral joints (p < 0.05). Fibroblasts derived from the contractive joints showed higher
mRNA and
protein expressions of CCT-eta in parallel with alpha-smooth muscle actin (α-SMA) compared to the cells from the contralateral knees (p < 0.05).
siRNA-mediated downregulation of CCT-eta inhibited the expressions of both CCT-eta and α-SMA. Moreover, the reduction of CCT-eta also significantly decreased fibroblast functions such as cell mobility and
collagen synthesis (all p < 0.05). Our findings indicate that CCT-eta appears to be a potential marker of joint
contracture disease.