PDF(Pubmed)
Abstract：
Fibrocartilaginous entheses consist of tendons, unmineralized and mineralized fibrocartilage, and subchondral bone, each exhibiting varying stiffness. Here we examined the functional role of sclerostin, expressed in mature mineralized fibrochondrocytes. Following rapid mineralization of unmineralized fibrocartilage and concurrent replacement of epiphyseal hyaline cartilage by bone, unmineralized fibrocartilage reexpanded after a decline in alkaline phosphatase activity at the mineralization front. Sclerostin was co-expressed with osteocalcin at the base of mineralized fibrocartilage adjacent to subchondral bone. In Scx-deficient mice with less mechanical loading due to defects of the Achilles tendon, sclerostin+ fibrochondrocyte count significantly decreased in the defective enthesis where chondrocyte maturation was markedly impaired in both fibrocartilage and hyaline cartilage. Loss of the Sost gene, encoding sclerostin, elevated mineral density in mineralized zones of fibrocartilaginous entheses. Atomic force microscopy analysis revealed increased fibrocartilage stiffness. These lines of evidence suggest that sclerostin in mature mineralized fibrochondrocytes acts as a modulator for mechanical tissue integrity of fibrocartilaginous entheses.
摘要：
纤维软骨组织由腱组成，未矿化和矿化的纤维软骨，和软骨下骨，每个都表现出不同的刚度。在这里，我们研究了硬化蛋白的功能作用，在成熟的矿化纤维软骨细胞中表达。在未矿化的纤维软骨快速矿化并同时由骨置换骨phy透明软骨后，矿化前沿碱性磷酸酶活性下降后，未矿化的纤维软骨重新扩张。硬化蛋白与骨钙蛋白在软骨下骨附近的矿化纤维软骨的底部共表达。在由于跟腱缺陷而导致机械负荷较低的Scx缺陷小鼠中，硬化蛋白纤维软骨细胞计数在有缺陷的胚胎中显着减少，其中软骨细胞成熟在纤维软骨和透明软骨中均明显受损。Sost基因的缺失,编码硬化蛋白，纤维软骨组织矿化区的矿物质密度升高。原子力显微镜分析显示纤维软骨硬度增加。这些证据表明，成熟的矿化纤维软骨细胞中的硬化蛋白可作为纤维软骨组织机械组织完整性的调节剂。
