Amano T, Muramatsu T, Amemiya K, Kubo K, Shimono M
Department of Pathology, Tokyo Dental College, Chiba, Japan.
J Dent Res. 2006 May;85(5):432-5. doi: 10.1177/154405910608500507.
Although heat stress can cause irritation in the dentin/pulp complex, little is known about the thermotolerance of pulp cells and their response to heat stress. We investigated cultured rat pulp cell responses to heat stress. Cells were subjected to a temperature of 42 degrees C for 30 minutes, and HSPs, alkaline phosphatase activity, and gap-junctional communication were determined at various time points. Although only low levels of HSP70 expression were detected before heat treatment, heat shock markedly induced HSP70 expression, with it gradually increasing at 1 hour after being heated. HSP25, however, showed no dramatic change. Gap junction protein connexin43 rapidly degraded after heat treatment, recovering to normal levels within the following 6 hours. Alkaline phosphatase activity decreased immediately after heat stress, recovering after 1 hour. These results indicate that dental pulp possesses protective factors, including HSPs, and that it can recover viability of intercellular communication and alkaline phosphatase activity after heat stress.
尽管热应激会导致牙本质/牙髓复合体产生刺激，但关于牙髓细胞的耐热性及其对热应激的反应却知之甚少。我们研究了培养的大鼠牙髓细胞对热应激的反应。将细胞置于42摄氏度的温度下30分钟，并在不同时间点测定热休克蛋白（HSPs）、碱性磷酸酶活性和缝隙连接通讯。尽管在热处理前仅检测到低水平的HSP70表达，但热休克显著诱导了HSP70的表达，在加热后1小时逐渐增加。然而，HSP25没有显著变化。热处理后缝隙连接蛋白连接蛋白43迅速降解，在接下来的6小时内恢复到正常水平。热应激后碱性磷酸酶活性立即下降，1小时后恢复。这些结果表明，牙髓拥有包括热休克蛋白在内的保护因子，并且在热应激后能够恢复细胞间通讯的活力和碱性磷酸酶活性。
