Continuous cyclic mechanical tension increases ank expression in endplate chondrocytes through the TGF-Î²1 and p38 pathway
AbstractThe normal ANK protein has a strong influence on anti-calcification. It is known that TGF-Î²1 is also able to induce extracellular inorganic pyrophosphate (ePPi) elaboration via the TGF-Î²1-induced ank gene expression and the mitogen-activated protein kinase (MAPK) signaling acts as a downstream effector of TGF-Î²1. We hypothesized that the expression of the ank gene is regulated by mechanics through TGF-Î²1-p38 pathway. In this study, we investigated the mechanism of short-time mechanical tension-induced ank gene expression. We found that the continuous cyclic mechanical tension (CCMT) increased the ank gene expression in the endplate chondrocytes, and there was an increase in the TGF-Î²1 expression after CCMT stimulation. The ank gene expression significantly increased when treated by TGF-Î²1 in a dose-dependent manner and decreased when treated by SB431542 (ALK inhibitor) in a dose-dependent manner. Our study results indicate that CCMT-induced ank gene expressions may be regulated by TGF-Î²1 and p38 MAPK pathway.
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Copyright (c) 2013 H. Xu, X. Zhang, H. Wang, Y. Zhang, Y. Shi, X. Zhang
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