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

Autor:	Lei Ding, Mengxuan Bian, Wei Lu, Qingmin Zeng, Zengxin Jiang, Defang Li, Jingping Wu
Jazyk:	angličtina
Rok vydání:	2020
Předmět:	Male 0301 basic medicine Cancer Research MAP Kinase Signaling System p38 mitogen-activated protein kinases Cell Apoptosis p38 Mitogen-Activated Protein Kinases Biochemistry cartilage endplate cell apoptosis Flow cytometry Rats Sprague-Dawley Gene Knockout Techniques 03 medical and health sciences Chondrocytes 0302 clinical medicine RNA interference Genetics medicine Animals p38/MAPK signalling pathway MALAT1 Molecular Biology Cells Cultured Oncogene medicine.diagnostic_test intervertebral disc degeneration Chemistry Articles Cell cycle Flow Cytometry Rats Cell biology Blot Cartilage Glucose 030104 developmental biology medicine.anatomical_structure Oncology 030220 oncology & carcinogenesis diabetes mellitus Molecular Medicine RNA Interference RNA Long Noncoding
Zdroj:	Molecular Medicine Reports
ISSN:	1791-3004 1791-2997
Popis:	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.
Databáze:	OpenAIRE
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