抄録
Core temperature of tendon is known to elevate to approximately 43°C under severe mechanical loading in horse as well as in human. This elevated temperature could be a potential etiology of tendinopathy; however, little is known about how hyperthermia affects tenocyte functions. Therefore, the present study hypothesized that such high temperature affects gap junction communication between tenocytes and upregulated tenocyte catabolism. Gap junction communication was evaluated using fluorescence loss in photobleaching (FLIP) protocol, with a mathematical model to estimate both intracellular and intercellular diffusion coefficients from FLIP result. It was exhibited that intercellular diffusion coefficient in tenocytes exposed to 43°C for 30 minutes was significantly larger than that in tenocytes exposed to 37°C. In addition, mRNA expression for catabolic markers, MMP-1 and IL-1β, was markedly upregulated but that for type I collagen was downregulated in 43°C treated group compared to 37°C treated group. Therefore, hyperthermia enhances gap junction communications and catabolic activities in tenocytes, suggesting that hyperthermia could be a trigger of inflammation response.
