The role and underlying mechanisms of microRNA‑214 in Legg‑Calvé‑Perthes disease Corrigendum in /10.3892/mmr.2019.10648

Zhu,Hui; Qi,Xinyue; Liu,Yuehe; Liao,Wei; Sun,Xiangshui; Tang,Yuping

doi:10.3892/mmr.2019.10271

The role and underlying mechanisms of microRNA‑214 in Legg‑Calvé‑Perthes disease

Corrigendum in: /10.3892/mmr.2019.10648

Authors:
- Hui Zhu
- Xinyue Qi
- Yuehe Liu
- Wei Liao
- Xiangshui Sun
- Yuping Tang
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Affiliations: Department of Orthopedics, Children's Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu 210009, P.R. China
Published online on: May 22, 2019 https://doi.org/10.3892/mmr.2019.10271
Pages: 685-692
Copyright : © Zhu et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].

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Abstract

Legg‑Calvé‑Perthes disease (LCPD) is a pediatric form of femoral head osteonecrosis with unknown etiology. MicroRNAs (miRs) have been revealed to serve an important role in LCPD. MiR‑214 serves an important role in chondrogenesis. The aim of the present study was to investigate the potential role of miR‑214 in LCPD and the underlying mechanisms. The expression levels of miR‑214 and B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax) in dexamethasone (DEX)‑treated TC28 cells, and the femoral head cartilage tissues, serum and primary chondrocytes of patients with LCPD, and healthy individuals were determined via reverse transcription quantitative polymerase chain reaction and western blot analysis. A luciferase reporter assay was conducted to investigate the association between miR‑214 and Bax, while cell viability was determined via an MTT assay, and flow cytometry was performed to investigate cell apoptosis. The results revealed that miR‑214 was downregulated and Bax was upregulated in DEX‑treated TC28 cells and tissues obtained from patients with LCPD. MiR‑214 was demonstrated to directly target Bax and negatively regulate its expression. DEX administration significantly suppressed cell proliferation, promoted apoptosis and decreased the Bcl‑2/Bax ratio in TC28 cells; overexpression of miR‑214 induced opposing effects, which were reversed by Bax overexpression. In conclusion, the results indicated that miR‑214 and Bax may be potential therapeutic targets for the future clinical treatment of LCPD.

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