Open AccessMicroRNA‑25‑3p regulates human nucleus pulposus cell proliferation and apoptosis in intervertebral disc degeneration by targeting Bim
Author(s) -
Zhigang Zhao,
Jie Zheng,
Youchen Ye,
Kai Zhao,
Ruozhang Wang,
Ran Wang
Publication year - 2020
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2020.11483
Subject(s) - apoptosis , microrna , microbiology and biotechnology , cell growth , cell , cell cycle , transfection , intervertebral disc , biology , oncogene , cancer research , chemistry , cell culture , anatomy , gene , biochemistry , genetics
Intervertebral disc degeneration (IDD) is a degenerative disease of the spine originating from the intervertebral disc. MicroRNAs (miRNAs or miRs) are a group of endogenous small non‑coding RNAs that act on target genes and play a critical role in numerous biological processes. However, the underlying mechanism of miR‑25‑3p in IDD remains unclear. Therefore, the present study aimed to explore the role of miR‑25‑3p in the pathogenesis of IDD. The results demonstrated that miR‑25‑3p was downregulated in rat degenerative nucleus pulposus (NP) cells and that Bcl‑2 interacting mediator of cell death (Bim) was a direct target of miR‑25‑3p. Next, to investigate the effect of miR‑25‑3p on normal NP cell proliferation and apoptosis, NP cells were transfected with an miR‑25‑3p inhibitor, a negative control of miR‑25‑3p inhibitor, miR‑25‑3p inhibitor + control‑small interference RNA (siRNA) or miR‑25‑3p inhibitor + Bim‑siRNA for 48 h and cell proliferation and apoptosis were then analyzed. The results demonstrated that the miR‑25‑3p inhibitor could decrease NP cell proliferation and induce cell apoptosis, and these effects were reversed by Bim‑siRNA. In addition, an in vitro cell model of IDD was established by subjecting NP cells to 10 ng/ml interleukin (IL)‑1β for 24 h. Further experiments suggested that IL‑1β treatment induced a reduction in NP cell proliferation and an increase in cell apoptosis, which were prevented by the miR‑25‑3p mimic. All the effects of miR‑25‑3p mimic on IL‑1β‑treated NP cells were significantly reversed by Bim upregulation. These findings suggested that miR‑25‑3p may be a novel therapeutic target for IDD prevention.