Role of lncRNA PART1 in intervertebral disc degeneration and associated underlying mechanism
- Zongyu Zhang
- Yongfeng Huo
- Zhijing Zhou
- Peng Zhang
- Jun Hu
Affiliations: Department of Orthopedics, Lianyungang Affiliated Hospital of Nanjing University of Chinese Medicine, Lianyungang Traditional Chinese Medicine Hospital, Lianyungang, Jiangsu 222004, P.R. China, Department of Orthopedics, The First Affiliated Hospital of Kangda College of Nanjing Medical University, Xuzhou Medical University Affiliated Hospital of Lianyungang, Lianyungang, Jiangsu 222004, P.R. China
- Published online on: December 10, 2020 https://doi.org/10.3892/etm.2020.9563
Copyright: © Zhang
et al. This is an open access article distributed under the
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Intervertebral disc degeneration (IDD) is a chronic skeletal muscle degeneration disease. Previous studies have demonstrated that long non‑coding RNAs (lncRNAs) exert significant roles in serious illnesses. Prostate androgen‑regulated transcript 1 (PART1) is an identified lncRNA that has been reported to be a regulator in a number of diseases. However, the potential effects of PART1 in IDD have yet to be fully elucidated. The present study aimed to investigate the roles of lncRNA PART1 in IDD and identify a possible underlying mechanism. Human nucleus pulposus (NP) cells were first exposed to lipopolysaccharide (LPS) to construct in vitro IDD models. Reverse transcription‑quantitative PCR (RT‑qPCR) was performed to measure lncRNA PART1 expression levels in 10 ng/ml LPS‑stimulated NP cells and normal cells (untreated cells). Dual‑luciferase reporter assays were conducted to verify the possible binding sites of microRNA (miR)‑190a‑3p on lncRNA PART1. In addition, NP cell viability and apoptosis were measured by performing MTT and flow cytometry, respectively. Expression and secretion of inflammatory factors (TNF‑α, IL‑1β and IL‑6) and extracellular matrix (ECM) degradation‑related proteins (aggrecan and collagen type II) were measured using ELISA, RT‑qPCR and western blotting. Expression levels of lncRNA PART1 in LPS‑treated NP cells were found to be higher compared with those in the control groups. miR‑190a‑3p directly targeted lncRNA PART1. PART1 knockdown enhanced cell viability, reduced cell apoptosis, inhibited inflammatory factor secretion and promoted ECM degradation in LPS‑stimulated NP cells. However, transfection with the miR‑190a‑3p inhibitor reversed the aforementioned PART1 knockdown‑induced alterations in cell viability, apoptosis, inflammatory cytokine and ECM degradation. Collectively, these results suggest that PART1 accelerates the progression of IDD by directly targeting miR‑190a‑3p, which provides a novel target for IDD diagnosis and treatment.