Thermal Preconditioning May Prevent Tendon Adhesion by Up-Regulating HSP72 in Rats

Abstract

Background/Aims: The study aims to determine the effects of thermal preconditioning on tendon adhesion by regulating the expression of heat shock protein 72 (HSP72) in rat models. Methods: Sixty male Wistar rats were collected and randomly assigned into the thermal preconditioning and control groups. During the 4^th and 8^th weeks following surgery, 15 rats were sacrificed in each period respectively, and their tendon adhesion was observed and evaluated. Biomechanical testing was performed to measure the tensile strength and gliding distance of tendons. Hematoxylin-eosin (HE) was used to observe the morphological structure of the tendons. Immunohistochemical staining, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used to detect the HSP72, fibroblast growth factor-2 (FGF-2), fibroblast growth factor receptor-1 (FGFR-1), β-catenin, epithelial cell adhesion molecule (EPCAM), Tenomodulin and scleraxis protein expressions. Pearson correlation analysis was applied to analyze the correlation between HSP72 expression and tendon adhesion. Results: At the 4^th week after surgery, we found no differences in the tendon adhesion scores or mRNA and protein expressions of HSP72 between the thermal preconditioning and control groups. However, after the 8^th week after surgery, the thermal preconditioning group had a lower tendon adhesion score and higher mRNA and protein expressions of HSP72 than the control group. During the same period, we found longer gliding distance and higher expression levels of FGF-2, FGFR-1, β-catenin, Tenomodulin and scleraxis, but lower EPCAM expression in the thermal preconditioning group. Pearson correlation analysis indicated that HSP72 mRNA and protein expression levels were negatively correlated with tendon adhesion. Conclusions: These findings provide evidence that thermal preconditioning may alleviate tendon adhesions via upregulation of HSP72 expression.

Thermal pretreatment promotes the protective effect of HSP70 against tendon adhesion in tendon healing by increasing HSP70 expression

“…In addition, as an anti-apoptotic chaperone and through its chaperone activity, HSP70 tightly regulates inflammatory responses via the nuclear factor-κβ signaling pathway, which is a critical pathway in mediating inflammatory responses (35). A previous study additionally demonstrated that TP reduced tendon adhesion via upregulating HSP72 expression (36). Furthermore, HSPs serve a substantial role in dealing with environmental stresses, including heat stress, whereas TP increases the mRNA levels of rhopalosiphum padi HSPs (37).…”

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