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

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Jianmin Xue ◽  
Baoyang Hu ◽  
Wenhua Xing ◽  
Feng Li ◽  
Zhi Huang ◽  
...  

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.

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Shangzhi Li ◽  
Jinwei Liu ◽  
Liang Chen

Abstract Background Intervertebral disk degeneration (IDD) is caused by nucleus pulposus (NP) degeneration and extracellular matrix (ECM) remodeling and cartilage intermediate layer protein (CILP) expression has been confirmed to be increased in IDD. This study is mainly conducted to clarify the mechanism of CILP in the NP cell degeneration and ECM remodeling in IDD. Methods CILP expression in the degenerated NP tissues and cells is quantified by quantitative real-time PCR and western blot. CILP function is assessed by cell cycle assay, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry, β-galactosidase staining, and the detection of ECM-related molecules aggrecan, collagen type I, collagen type II, MMP-3, and MMP-9 expression is accomplished by qRT-PCR. The potential mechanism is authenticated by dual-luciferase reporter gene assay. Results CILP was increased in the degenerated NP tissues and cells, and the knockdown of CILP promoted the NP cell cycle, increased cell activity, and repressed cell apoptosis and repressed cell senescence and ECM production. Moreover, miR-330-5p targeted the CILP 3′-untranslated region, and miR-330-5p negatively regulated CILP expression. Moreover, the overexpression of miR-330-5p repressed NP cell degeneration and ECM remodeling to relieve IDD by downregulating CILP. Conclusion MiR-330-5p represses NP cell degeneration and ECM remodeling to ameliorate IDD by downregulating CILP.


2012 ◽  
Vol 2 (1_suppl) ◽  
pp. s-0032-1319972-s-0032-1319972
Author(s):  
T. Law ◽  
M. P. Anthony ◽  
D. Samartzis ◽  
Q. Chan ◽  
M. Kim ◽  
...  

2012 ◽  
Vol 2 (1_suppl) ◽  
pp. s-0032-1319873-s-0032-1319873
Author(s):  
P. Colombier ◽  
J. Clouet ◽  
E. Miot-Noirault ◽  
A. Vidal ◽  
F. Cachin ◽  
...  

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Qi Sun ◽  
Xin-Yu Nan ◽  
Fa-Ming Tian ◽  
Fang Liu ◽  
Shao-Hua Ping ◽  
...  

Abstract Background Adjacent segmental intervertebral disk degeneration (ASDD) is a major complication secondary to lumbar fusion. Although ASSD pathogenesis remains unclear, the primary cause of intervertebral disk degeneration (IVDD) development is apoptosis of nucleus pulposus (NP). Raloxifene (RAL) could delay ASDD by inhibiting NP apoptosis. Methods An ASDD rat model was established by ovariectomy (OVX) and posterolateral spinal fusion (PLF) on levels 4–5 of the lumbar vertebrae. Rats in the treatment groups were administered 1 mg/kg/d RAL by gavage for 12 weeks, following which, all animals were euthanized. Lumbar fusion, apoptosis, ASDD, and vertebrae micro-architecture were evaluated. Results RAL maintained intervertebral disk height (DHI), delayed vertebral osteoporosis, reduced histological score, and inhibited apoptosis. The OVX+PLF+RAL group revealed upregulated expression of aggrecan and B-cell lymphoma-2 (bcl2), as well as significantly downregulated expression of a disintegrin and metalloproteinase with thrombospondin motifs 4 (ADAMTS-4), metalloproteinase-13 (MMP-13), caspase-3, BCL2-associated X (bax), and transferase dUTP nick end labeling (TUNEL) staining. Micro-computed tomography (Micro-CT) analysis revealed higher bone volume fraction (BV/TV), bone mineral density (BMD), and trabecular number (Tb.N), and lower trabecular separation (Tb.Sp) in OVX+PLF+RAL group than in the OVX+PLF group. Conclusions RAL can postpone ASDD development in OVX rats through inhibiting extracellular matrix metabolic imbalance, NP cell apoptosis, and vertebral osteoporosis. These findings showed RAL as a potential therapeutic target for ASDD.


2011 ◽  
Vol 30 (6) ◽  
pp. 950-957 ◽  
Author(s):  
Lucas A. Smolders ◽  
Björn P. Meij ◽  
Frank M. Riemers ◽  
Ruud Licht ◽  
Richard Wubbolts ◽  
...  

2017 ◽  
Vol 30 (5) ◽  
pp. E547-E553 ◽  
Author(s):  
Akinobu Suzuki ◽  
Michael D. Daubs ◽  
Tetsuo Hayashi ◽  
Monchai Ruangchainikom ◽  
Chenjie Xiong ◽  
...  

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