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

Hongguang Xu | Zendy; X. Zhang | Zendy; Hongshun Wang | Zendy; Y. Zhang | Zendy; Yu Shi | Zendy

Open Access

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

Author(s) -

Hongguang Xu,

X. Zhang,

Hongshun Wang,

Y. Zhang,

Yu Shi

Publication year - 2013

Publication title -

european journal of histochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.754

H-Index - 42

eISSN - 2038-8306

pISSN - 1121-760X

DOI - 10.4081/ejh.2013.e28

Subject(s) - chemistry , microbiology and biotechnology , transforming growth factor , tension (geology) , biophysics , anatomy , biology , materials science , composite material , ultimate tensile strength

The normal ANK protein has a strong influence on anti-calcification. It is known that TGF-β1 is also able to induce extracellular inorganic pyrophosphate (ePPi) elaboration via the TGF-β1-induced ank 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 ank gene is regulated by mechanics through TGF-β1-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-β1 expression after CCMT stimulation. The ank 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 ank gene expressions may be regulated by TGF-β1 and p38 MAPK pathway.

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