Continuous cyclic mechanical tension increases ank expression in endplate chondrocytes through the TGF-β1 and p38 pathway

The normal ANK protein has a strong influence on anti-calcification. It is known that <em>TGF-β1</em> is also able to induce extracellular inorganic pyrophosphate (ePPi) elaboration via the TGF-β1-induced <em>ank</em> gene expression and the mitogen-activated protein kinase (MAPK) signaling acts as a downstream effector of TGF-β1. We hypothesized that the expression of the <em>ank</em> gene is regulated by mechanics through TGF-β1-p38 pathway. In this study, we investigated the mechanism of short-time mechanical tension-induced <em>ank</em> gene expression. We found that the continuous cyclic mechanical tension (CCMT) increased the <em>ank</em> gene expression in the endplate chondrocytes, and there was an increase in the TGF-β1 expression after CCMT stimulation. The <em>ank</em> gene expression significantly increased when treated by TGF-β1 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 <em>ank</em> gene expressions may be regulated by TGF-β1 and p38 MAPK pathway.<br />

Abstract licence: CC BY-NC

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