Continuous cyclic mechanical tension increases ank expression in endplate chondrocytes through the TGF-?1 and p38 pathway.

ABSTRACT: The normal ANK protein has a strong influence on anti-calcification. It is known that TGF-?1 is also able to induce extracellular inorganic pyrophosphate (ePPi) elaboration via the TGF-?1-induced ank gene expression and the mitogen-activated protein kinase (MAPK) signaling acts as a downstream effector of TGF-?1. We hypothesized that the expression of the ank gene is regulated by mechanics through TGF-?1-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-?1 expression after CCMT stimulation. The ank gene expression significantly increased when treated by TGF-?1 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-?1 and p38 MAPK pathway.

SUBMITTER: Xu H 

PROVIDER: S-EPMC3794359 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature