Long non‑coding RNA MALAT1 promotes high glucose‑induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway

Jiang,Zengxin; Zeng,Qingmin; Li,Defang; Ding,Lei; Lu,Wei; Bian,Mengxuan; Wu,Jingping

doi:10.3892/mmr.2020.11009

Long non‑coding RNA MALAT1 promotes high glucose‑induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway

Authors:
- Zengxin Jiang
- Qingmin Zeng
- Defang Li
- Lei Ding
- Wei Lu
- Mengxuan Bian
- Jingping Wu
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Affiliations: Department of Orthopedic Surgery, Fudan University Jinshan Hospital, Shanghai 201508, P.R. China, Department of Orthopedic Surgery, Shanghai TCM‑Integrated Hospital, Shanghai University of TCM, Shanghai 200082, P.R. China
Published online on: March 3, 2020 https://doi.org/10.3892/mmr.2020.11009
Pages: 2220-2226
Copyright: © Jiang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Diabetes mellitus (DM) contributes to intervertebral disc degeneration (IDD). The long non‑coding RNA MALAT1 has been revealed to play an important role in diabetes‑associated complications. However, the specific role of MALAT1 in diabetes‑associated IDD has not been determined. The aim of the present study was to evaluate the roles of MALAT1 in the apoptosis of cartilage endplate (CEP) cells induced by high glucose and to explore the mechanisms underlying this effect. Rat CEP cells were cultured in high‑glucose medium (25 mM glucose) for 24 or 72 h. Cells cultured in medium containing 5 mM glucose were used as a control. Flow cytometry was used to detect the degree of apoptosis. Reverse transcription‑quantitative PCR was used to measure the expression of MALAT1 mRNA. In addition, CEP cells were treated with different conditions (high glucose, high glucose + MALAT1 negative control, high glucose + MALAT1 RNAi, normal control) for 72 h. Flow cytometry was subsequently used to detect apoptosis and western blotting was used to measure the expression levels of total and phosphorylated p38. The results revealed that high glucose concentration promoted apoptosis and enhanced expression of MALAT1 in CEP cells. Furthermore, MALAT1 knockout decreased the expression levels of total and phosphorylated p38 and reduced the apoptosis of rat CEP cells. The results obtained in the present study indicated that MALAT1 may serve as an important therapeutic target for curing or delaying IDD in patients with diabetes.

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