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. 2020 Sep;22(9):e3203.
doi: 10.1002/jgm.3203. Epub 2020 May 1.

LncRNA NEAT1 promotes proliferation of chondrocytes via down-regulation of miR-16-5p in osteoarthritis

Dan Li  1 , Yongjin Sun  2 , Yunpeng Wan  3 , Xing Wu  4 , Wanrong Yang  1
Affiliations

LncRNA NEAT1 promotes proliferation of chondrocytes via down-regulation of miR-16-5p in osteoarthritis

Dan Li et al. J Gene Med. 2020 Sep.

Abstract

Background: Non-coding RNAs are endogenous regulators of gene expression that have been implicated in the pathogenesis of various diseases, including osteoarthritis (OA). Long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) and miR-16-5p are up-regulated in OA tissues; however, their functions have not been clarified.

Methods: Chondrocyte ATDC5 was used as a cell model. NEAT1 overexpression and knockdown cells were established by transfection with lipofectamine. miR-16-5p was also transfected into the cells using lipofectamine. Moreover, cell proliferation was examined using cell counting kit-8 assays. Cell apoptosis was evaluated by flow cytometry. The interaction between NEAT1 and miR-16-5p was validated by a Quantitative real-time RT-PCR (qRT-PCR) and dual-luciferase reporter assays.

Results: NEAT1 could increase cell viability and decrease apoptosis of ATDC5 cells, whereas miR-16-5p had the opposite effects. NEAT1 could specifically bind to miR-16-5p and reduce its expression.

Conclusions: The suppression of miR-16-5p, as mediated by NEAT1 overexpression, could promote proliferation and inhibit apoptosis of chondrocytes. It was also revealed that NEAT1 is a "double-edged sword" during the development of OA.

Keywords: ATDC5; NEAT1; OA; apoptosis; miR-16-5p; proliferation.

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References

REFERENCES

    1. Hermann W, Lambova S, Muller-Ladner U. Current treatment options for osteoarthritis. Curr Rheumatol Rev. 2018;14:108-116.
    1. Robinson WH, Lepus CM, Wang Q, et al. Low-grade inflammation as a key mediator of the pathogenesis of osteoarthritis. Nat Rev Rheumatol. 2016;12:580-592.
    1. Pearle AD, Warren RF, Rodeo SA. Basic science of articular cartilage and osteoarthritis. Clin Sports Med. 2005;24:1-12.
    1. Marques-Rocha JL, Samblas M, Milagro FI, Bressan J, Martínez JA, Marti A. Noncoding RNAs, cytokines, and inflammation-related diseases. FASEB j. 2015;29:3595-3611.
    1. Ma H, Han P, Ye W, et al. The long noncoding RNA NEAT1 exerts antihantaviral effects by acting as positive feedback for RIG-I signaling. J Virol. 2017;91(9):e02250-16.

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