Investigating conversion of endplate chondrocytesinduced by intermittent cyclic mechanical unconfinedcompression in three-dimensional cultures

Mechanical stimulation is known to regulate the calcification of endplate chondrocytes. The Ank protein has a strong influence on anti-cal-cification by transports intracellular inorganic pyrophosphate (PPi) to the extracellular matrix. It is known that TGF-1 is able to induce Ank gene expression and protect chondrocyte calci-fication. Intermittent cyclic mechanical tension (ICMT) could induce calcification of endplate chondrocytes by decrease the expression of Ank gene. In this study, we investigated the relation of intermittent cyclic mechanical unconfined compression (ICMC) and Ank gene expression. We found that ICMC decreased the Ank gene expression in the endplate chondrocytes, and there was an decreased in the TGF-1 expres-sion after ICMC stimulation. The Ank gene expression significantly increased when treated by transforming growth factor alpha 1 (TGF-1) in a dose-dependent manner and decreased when treated by SB431542 (ALK inhibitor) in a dose-dependent manner. Our results implicate that ICMC-induced downregulation of Ank gene expression may be regulated by TGF-1 in end-plate chondrocytes