LncRNA MEG3 inhibits proliferation and promotes apoptosis of synovial cells in rats with knee osteoarthritis by regulating PTEN

K. Han, F.-R. Wang, M.-Q. Yu, B. Xu

Department of Traumatic Orthopaedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China. sdslyygkhk@126.com

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• Orthopedics

OBJECTIVE: To study the influences of long non-coding ribonucleic acid (lncRNA) maternally expressed gene 3 (MEG3) on the proliferation and apoptosis of synovial cells in rats with knee osteoarthritis by regulating phosphate and tension homology deleted on chromosome ten (PTEN).

MATERIALS AND METHODS: In this experiment, rat synovial cell (RSC)-364 cells were cultured in vitro. Then, they were treated with PBS or lncRNA MEG3 overexpression lentiviruses and divided into normal control (NC) group and lncRNA MGE3 overexpression group (LncRNA MEG3 group). The messenger RNA (mRNA) expression levels of lncRNA MEG3 and PTEN in rat synovial cells were measured via qRT-PCR in each group, and Western blotting (WB) was performed to determine the protein levels of PTEN, cyclin D1, P21, B-cell lymphoma 2 (Bcl-2) and tubulin in rat synovial cells in both groups. The proliferation of rat synovial cells was detected via MTT assay, and the apoptosis was evaluated using FITC/PI double staining and flow cytometer.

RESULTS: Compared with NC group, LncRNA MEG3 group had notably overexpressed lncRNA MEG3 in RSC-364 cells (p<0.01), and an extremely substantially elevated mRNA level of PTEN (p<0.05). Besides, it was found through WB that the protein expression level of PTEN had a consistent trend with that of the mRNA level. The proliferation ability of cells was weakened (p<0.05), and the number of apoptotic cells was increased (p<0.05) in LncRNA MEG3 group compared with those in NC group. Finally, LncRNA MEG3 group had remarkably lower protein levels of cyclin D1 and Bcl-2, but a markedly higher protein level of P21 than NC group (p<0.05).

CONCLUSIONS: LncRNA MEG3 can raise the level of PTEN to weaken the proliferation ability but elevate the apoptosis level of RSC-364 cells.

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