circRNA_0058097 promotes tension‐induced degeneration of endplate chondrocytes by regulating HDAC4 expression through sponge adsorption of miR‐365a‐5p
Excessive mechanical tension can lead to the degeneration of endplate chondrocytes. The presence of tension‐sensitive circRNA_0058097 molecules has been detected in human endplate chondrocytes, where it was found to be a potential competing endogenous RNA. Indeed, inhibiting the expression of circRN...
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Published in | Journal of cellular biochemistry Vol. 121; no. 1; pp. 418 - 429 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Wiley Subscription Services, Inc
01.01.2020
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Subjects | |
Online Access | Get full text |
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Summary: | Excessive mechanical tension can lead to the degeneration of endplate chondrocytes. The presence of tension‐sensitive circRNA_0058097 molecules has been detected in human endplate chondrocytes, where it was found to be a potential competing endogenous RNA. Indeed, inhibiting the expression of circRNA_0058097 effectively enhanced the stress resistance of endplate chondrocytes, suggesting that it may be an important trigger point for the degeneration of endplate cartilage. Through a series of experiments, we reveal that circRNA_0058097 can upregulate the expression of downstream target gene histone deacetylase 4 by sponge adsorption of miR‐365a‐5p, which promoted morphological changes of endplate chondrocytes, and increased extracellular matrix degradation and degeneration of endplate cartilage. Therefore, circRNA_0058097 may provide a new way to prevent and treat endplate cartilage degeneration.
Excessive intermittent cyclic mechanical tension can induce the degeneration of endplate chondrocytes. Tension‐sensitive circRNA_0058097 can upregulate the expression of downstream target gene histone deacetylase 4 by sponge adsorption of miR‐365a‐5p, which promoted morphological changes of endplate chondrocytes, and increased extracellular matrix degradation and degeneration of endplate cartilage. |
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Bibliography: | Liang Xiao, Baiyang Ding, and Shujuan Xu contributed equally to this study. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0730-2312 1097-4644 |
DOI: | 10.1002/jcb.29202 |