Ann Clin Case Rep | Volume 7, Issue 1 | Research Article | Open Access

LncRNA SNHG1 Alleviates the IL-1β-Induced Chondrocytes Inflammatory Injury via Targeting miR-143- 3p/KLF2 Axis

Lang Liu1,2,3,4, Jiayu Huang2,3,4, Feng Cai2,3, Qincan Chen2,4, Sijie Xia2,4 and Qi Liao1,2,3*

1Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The Third Affiliated Hospital of Nanchang University, Nanchang, China 2Department of Orthopedics, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China 3Nanchang Key Laboratory of Orthopaedics, The Third Affiliated Hospital of Nanchang University, Nanchang, China 4Medical Department of Graduate School, Nanchang University, Nanchang, Jiangxi 330006, China

*Correspondance to: Qi Liao 

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Abstract

Background: Osteoarthritis (OA), a chronic degenerative joint disease, is short of definitive therapeutic methods until now. More and more studies showed that long non-coding RNAs (lncRNAs) performed essential roles in OA. This study is aimed at investigating the effect of lncRNA SNHG1 on IL-1β-stimulated chondrocytes inflammatory injury in mice. Materials and Method: As the latest studies indicated, the mouse chondrocytes, stimulated by IL-1β, were used for constructing a model of inflammatory injury. The functions of SNHG1 overexpression or inhibition in regulating apoptosis, inflammation and Extracellular Matrix (ECM) in IL-1β injured chondrocytes were evaluated. Then, bioinformatics methods were used to screen possible targets of SNHG1, and the relationships among SNHG1, miRNA-143-3p, and Kruppel Like Factor 2 (KLF2) were verified by qRT-PCR and luciferase reporter gene assays. Furthermore, the functional mechanism of SNHG1 was explored through miR-143-3p overexpressed or the knockdown of KLF2 as recovery experiments. Results: SNHG1 was reduced in mouse chondrocytes stimulated by IL-1β. Moreover, overexpression of SNHG1 reduced apoptosis inhibited the inflammatory response and the degradation of ECM. Mechanistically, SNHG1, which functions as a sponger, directly bound to miRNA-143-3p. Additionally, transfection of miRNA-143-3p mimics reversed the inhibition of apoptosis and ECM degradation exerted by SNHG1 overexpression. SNHG1 exerted its function by indirectly regulating KLF2, a downstream target of miRNA-143-3p. Conclusion: Our study demonstrated that lncRNA SNHG1 protected chondrocytes against IL-1β- stimulated inflammatory injury by targeting miRNA-143-3p/KLF2 axis. It is suggested that SNHG1 might be a potential therapeutic target in OA.

Keywords:

MicroRNAs; Osteoarthritis; Long non-coding; SNHG1

Citation:

Liu L, Huang J, Cai F, Chen Q, Xia S, Liao Q. LncRNA SNHG1 Alleviates the IL-1β-Induced Chondrocytes Inflammatory Injury via Targeting miR- 143-3p/KLF2 Axis. Ann Clin Case Rep. 2022; 7: 2179..

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