Papachristou Dionysios J, Papadakou Eugenia, Basdra Efthimia K, Baltopoulos Panagiotis, Panagiotopoulos Elias, Papavassiliou Athanasios G
Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA, USA.
Mol Med. 2008 Mar-Apr;14(3-4):160-6. doi: 10.2119/2007-00138.Papachristou.
Meniscal tears are attributed to either trauma or degeneration processes. Clinical data suggest that meniscal degeneration (MD) is associated with knee osteoarthritis; however, the molecular events underpinning the pathogenesis of MD in humans remain elusive. Here we immunohistochemically examined the expression of p38 MAPK, its phosphorylated/activated form (p-p38), its target NF-kappaB (p50-p65 dimer), and COX-2 in ruptured menisci and investigated their involvement in MD development. Our findings demonstrate increased expression of the p38-NF-kappaB axis elements and COX-2 in disintegrated fibrocartilage, suggesting a role of these molecules in the pathobiochemistry of MD and consequential rupture.
半月板撕裂归因于创伤或退变过程。临床数据表明，半月板退变（MD）与膝关节骨关节炎相关；然而，人类MD发病机制背后的分子事件仍不清楚。在此，我们通过免疫组织化学方法检测了破裂半月板中p38丝裂原活化蛋白激酶（p38 MAPK）、其磷酸化/活化形式（p-p38）、其靶标核因子κB（p50-p65二聚体）和环氧化酶-2（COX-2）的表达，并研究了它们在MD发展中的作用。我们的研究结果表明，在崩解的纤维软骨中，p38-核因子κB轴元件和COX-2的表达增加，提示这些分子在MD的病理生物化学及随后的破裂中发挥作用。
