1. Academic Validation
  2. Low expression of miR-142-3p promotes intervertebral disk degeneration

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

  • J Orthop Surg Res. 2021 Jan 14;16(1):55. doi: 10.1186/s13018-020-02194-4.
Jianmin Xue  # 1 2 Baoyang Hu  # 1 2 Wenhua Xing 2 Feng Li 2 Zhi Huang 2 Wenkai Zheng 2 Bo Wang 1 2 Yong Zhu 3 Xuejun Yang 4
Affiliations

Affiliations

  • 1 Graduate School of Inner Mongolia Medical University, Hohhot City, 010059, Inner Mongolia, China.
  • 2 Department of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China.
  • 3 Department of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China. [email protected].
  • 4 Department of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China. [email protected].
  • # Contributed equally.
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.

Keywords

Cell behavior; Intervertebral disk degeneration; miR-142-3p.

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