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Investigating conversion of endplate chondrocytes induced by intermittent cyclic mechanical unconfined compression in three-dimensional cultures
Mechanical stimulation is known to regulate the calcification of endplate chondrocytes. The ANK protein has a strong influence on anti-calcification by transports intracellular inorganic pyrophosphate (PPi) to the extracellular. It is known that TGF-β1 is able to induced Ank gene expression and protect chondrocyte calcification. 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-β1 expression after ICMC stimulation. The Ank gene expression significantly increased when treated by transforming growth factor alpha 1 (TGF-β1) 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-β1 in endplate chondrocytes.
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Citations
10.1016/j.heliyon.2024.e31162
10.1007/s13577-023-00959-7
10.1186/s13018-025-05577-7
10.1002/jcb.29202
10.3969/j.issn.1005-202X.2022.04.020
10.16156/j.1004-7220.2021.04.023
10.4081/ejh.2017.2762
10.4081/ejh.2016.2758
10.1007/s11926-016-0574-z
10.4081/ejh.2015.2610
10.4081/ejh.2014.2474
Supporting Agencies
Chinese National Natural Sciences Fund Project, Chinese Anhui Province Natural Science Fund ProjectHow to Cite
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