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Low expression of miR-142-3p promotes intervertebral disk degeneration.

Authors :
Xue, Jianmin
Hu, Baoyang
Xing, Wenhua
Li, Feng
Huang, Zhi
Zheng, Wenkai
Wang, Bo
Zhu, Yong
Yang, Xuejun
Source :
Journal of Orthopaedic Surgery & Research. 1/14/2021, Vol. 16 Issue 1, p1-10. 10p.
Publication Year :
2021

Abstract

Background: Intervertebral disk degeneration (IDD) is a degenerative disease characterized by cytoplasm loss and extracellular matrix degradation. Numerous evidence reported that miRNAs participated in IDD development. Nevertheless, the function of miR-142-3p in IDD development remains unknown. This study mainly explored the potential role and function of miR-142-3p in IDD development. Methods: One percent fetal bovine serum was used to induce the degeneration of ATDC5 cells, and miR-142-3p level was examined by qRT-PCR. Then, miR-142-3p mimic/inhibitor and its corresponding negative control were transfected into ATDC5 normal and degenerative cells. Viability, migration, invasion, apoptosis, cycle, Bax, Bcl-2, P62, and Beclin1 expression levels were assessed using CCK8, wound healing assay, annexin V-FITC/PI staining, western blot, and qRT-PCR, respectively. Results: The results revealed that the expression levels of MMP13, ADAMTS5, MMP3, and Col-X were increased as well as the expression levels of SOX-9 and Col-II were reduced in ATDC5 degenerative cells, indicating the degeneration model was constructed. We observed that miR-142-3p was decreased in ATDC5 degenerative cells and its suppression could promote ATDC5 cell degeneration. However, miR-142-3p overexpression could reverse the cell viability inhibition, as well as apoptosis and autophagy enhancement in ATDC5 degenerative cells. Conclusions: Our results proved that miR-142-3p may play an important role in disk degeneration. Further animal study is needed to illustrate the role of the miR-142-3p in IDD development. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
1749799X
Volume :
16
Issue :
1
Database :
Academic Search Index
Journal :
Journal of Orthopaedic Surgery & Research
Publication Type :
Academic Journal
Accession number :
148113128
Full Text :
https://doi.org/10.1186/s13018-020-02194-4