The TMSB4 Pseudogene LncRNA Functions as a Competing Endogenous RNA to Promote Cartilage Degradation in Human Osteoarthritis

Mechanical stress plays a key role in the development of cartilage degradation in osteoarthritis (OA). Nevertheless, the role of long noncoding RNAs in mechanical stress-induced regulation of chondrocytes remains unclear. The aim of this study was to explore the function of mechanical stress-related...

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Bibliographic Details
Published in:Molecular therapy 2016-10, Vol.24 (10), p.1726-1733
Main Authors: Liu, Qiang, Hu, Xiaoqing, Zhang, Xin, Dai, Linghui, Duan, Xiaoning, Zhou, Chunyan, Ao, Yingfang
Format: Article
Language:English
Subjects:
Arthritis
Cartilage
Cartilage, Articular - metabolism
Cartilage, Articular - pathology
Cells, Cultured
Cytoskeleton
Gene Expression Profiling
Genes
Humans
Matrix Metalloproteinases - genetics
MicroRNAs
MicroRNAs - genetics
Oligonucleotide Array Sequence Analysis
Original
Osteoarthritis
Osteoarthritis - genetics
Osteoarthritis - pathology
Polymerization
Proteins
RNA, Long Noncoding - genetics
Sports injuries
Sports medicine
Stress, Mechanical
Thymosin - genetics
Up-Regulation
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Summary:Mechanical stress plays a key role in the development of cartilage degradation in osteoarthritis (OA). Nevertheless, the role of long noncoding RNAs in mechanical stress-induced regulation of chondrocytes remains unclear. The aim of this study was to explore the function of mechanical stress-related long noncoding RNAs in cartilage. Tissue samples were collected from 50 patients and chondrocytes were exposed to cyclic tensile strain (CTS). A total of 107 lncRNAs were differentially expressed in damaged cartilage versus intact cartilage. Of these lncRNAs, 51 were upregulated and 56 were downregulated in the damaged tissue. The TMSB4 pseudogene, lncRNA-MSR, was upregulated in the damaged cartilage and was activated in chondrocytes in response to mechanical stress. Furthermore, lncRNA-MSR regulated the expression of TMSB4 by competing with miRNA-152 in chondrocytes. Our results demonstrated that upregulation of lncRNA-MSR initiates pathological changes that lead to cartilage degradation, and the inhibition of lncRNA-MSR could represent a potential therapeutic target for OA.
ISSN:1525-0016
1525-0024
DOI:10.1038/mt.2016.151