Wu M J, Lu H P, Gu Z Y, Zhou Y Q
Department of Orthodontics, Hospital of Stomatology, Zhejiang University, Hangzhou, China.
School of Stomatology, Zhejiang Chinese Medical University, Hangzhou, China.
Genet Mol Res. 2016 Jun 20;15(2):gmr7499. doi: 10.4238/gmr.15027499.
Abnormal pressure is an important factor that contributes to bone adaptation in the temporomandibular joint (TMJ). We determined the effect of the mitogen-activated protein kinases (MAPK) pathway on the pressure-induced synovial metaplasia procedure for the TMJ, both in vitro and in vivo. Synovial fibroblasts (SFs) were exacted from rat TMJs and exposed to different hydrostatic pressures. The protein extracts were analyzed to determine the activation of ERK1/2, JNK, and p38. Surgical anterior disc displacement (ADD) was also performed on Japanese rabbits, and the proteins of TMJ were isolated to analyze pressure-induced MAPK activation after 1, 2, 4, and 8 weeks. The results showed that the activation of ERK1/2 and JNK in SFs significantly changed with increasing hydrostatic pressure, whereas p38 activation did not change. Moreover, p38 was activated in animals 1 week after surgical ADD. The levels of p38 gradually increased after 2 and 4 weeks, and then slightly decreased but remained higher than in the control 8 weeks after surgical ADD. Nevertheless, JNK was rarely activated after the ADD treatment. Our findings suggest the involvement of MAPK activation in the pressure-induced synovial metaplasia procedure with pressure loading in TMJ.
异常压力是导致颞下颌关节（TMJ）骨适应性变化的一个重要因素。我们在体外和体内确定了丝裂原活化蛋白激酶（MAPK）通路对TMJ压力诱导滑膜化生过程的影响。从大鼠TMJ中提取滑膜成纤维细胞（SFs），并使其暴露于不同的静水压力下。分析蛋白质提取物以确定ERK1/2、JNK和p38的激活情况。对日本白兔进行手术性前盘移位（ADD），并在1、2、4和8周后分离TMJ的蛋白质，以分析压力诱导的MAPK激活情况。结果表明，随着静水压力的增加，SFs中ERK1/2和JNK的激活情况显著变化，而p38的激活情况没有改变。此外，在手术性ADD后1周，动物体内的p38被激活。2周和4周后，p38水平逐渐升高，然后略有下降，但在手术性ADD后8周仍高于对照组。然而，ADD治疗后JNK很少被激活。我们的研究结果表明，MAPK激活参与了TMJ压力加载诱导的滑膜化生过程。
