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 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 effec...
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| Format: | Online |
| Language: | English |
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PAGEPress Publications, Pavia, Italy
2013
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3794359/ |
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pubmed-37943592013-10-21 Continuous Cyclic Mechanical Tension Increases Ank Expression in Endplate Chondrocytes Through the TGF-β1 and p38 Pathway Xu, H. Zhang, X. Wang, H. Zhang, Y. Shi, Y. Zhang, X. Original Paper 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. PAGEPress Publications, Pavia, Italy 2013-09-29 /pmc/articles/PMC3794359/ /pubmed/24085277 http://dx.doi.org/10.4081/ejh.2013.e28 Text en ©Copyright H. Xu et al. http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Xu, H. Zhang, X. Wang, H. Zhang, Y. Shi, Y. Zhang, X. |
| spellingShingle |
Xu, H. Zhang, X. Wang, H. Zhang, Y. Shi, Y. Zhang, X. Continuous Cyclic Mechanical Tension Increases Ank Expression in Endplate Chondrocytes Through the TGF-β1 and p38 Pathway |
| author_facet |
Xu, H. Zhang, X. Wang, H. Zhang, Y. Shi, Y. Zhang, X. |
| author_sort |
Xu, H. |
| title |
Continuous Cyclic Mechanical Tension Increases Ank Expression in Endplate Chondrocytes Through the TGF-β1 and p38 Pathway |
| title_short |
Continuous Cyclic Mechanical Tension Increases Ank Expression in Endplate Chondrocytes Through the TGF-β1 and p38 Pathway |
| title_full |
Continuous Cyclic Mechanical Tension Increases Ank Expression in Endplate Chondrocytes Through the TGF-β1 and p38 Pathway |
| title_fullStr |
Continuous Cyclic Mechanical Tension Increases Ank Expression in Endplate Chondrocytes Through the TGF-β1 and p38 Pathway |
| title_full_unstemmed |
Continuous Cyclic Mechanical Tension Increases Ank Expression in Endplate Chondrocytes Through the TGF-β1 and p38 Pathway |
| title_sort |
continuous cyclic mechanical tension increases ank expression in endplate chondrocytes through the tgf-β1 and p38 pathway |
| description |
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. |
| publisher |
PAGEPress Publications, Pavia, Italy |
| publishDate |
2013 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3794359/ |
| _version_ |
1612017524548829184 |