CircRNA_0092516 regulates chondrocyte proliferation and apoptosis in osteoarthritis through the miR-337-3p/PTEN axis.

Zhihui Huang,Weiqi Ling,Wenming Ma,Jinhuai Xiao,Xiaoyu Dai

doi:10.1093/jb/mvaa119

Abstract

The dysregulation of circular RNAs (circRNAs) has been identified in various human diseases. Here, we probed into the potential mechanism of circRNA_0092516 in osteoarthritis (OA). The expression of circRNA_0092516 was tested by quantitative real-time PCR. MTT, flow cytometry and western blot were applied to confirm the functions of circRNA_0092516 in vitro. Besides, RNA pull-down and dual-luciferase reporter gene experiments were applied to probe into the mechanism. circRNA_0092516 was raised in the tissues of OA patients and chondrocytes stimulated by IL-1β. The potential mechanism analysis expounded that circRNA_0092516 bound to miR-337-3p, and the interference with circRNA_0092516 boosted chondrocyte proliferation and restrained cell apoptosis through the miR-337-3p/phosphatase and tensin homolog (PTEN) axis, thereby improving OA. In-vivo experiments expounded that circRNA_0092516 regulated cartilage production through miR-337-3p. Overall, our data expounded that the interference with circRNA_0092516 boosted chondrocyte proliferation and restrained cell apoptosis through the miR-337-3p/PTEN axis, eventually slowed down the progress of OA.

Highlights

Osteoarthritis (OA) is a type of age-related joint disease that has been widely regarded as an irreversible disease and one of the main causes of disability in the elderly[1]
We urgently need to explore the underlying mechanism of chondrocyte proliferation and apoptosis in OA, which is critical for the relief of OA
Increasing evidence shows that circRNAs are rich in the binding sites of miRNAs, and affect the expression of downstream target mRNA by competing for endogenous RNA to interact with miRNA[11, 12]

Summary

Introduction

Osteoarthritis (OA) is a type of age-related joint disease that has been widely regarded as an irreversible disease and one of the main causes of disability in the elderly[1]. Increasing evidence indicates that the dysregulation of circRNAs is closely related to the progress of various human diseases. Shen et al indicated that the overexpression of circSERPINE2 impedes the progression of OA by inhibiting human chondrocyte apoptosis[9]. Increasing evidence shows that circRNAs are rich in the binding sites of miRNAs, and affect the expression of downstream target mRNA by competing for endogenous RNA (ceRNA) to interact with miRNA[11, 12]. It is currently unclear whether circRNA_0092516 can act as a ceRNA in the progress of OA. We mainly investigated the potential mechanism of circRNA_0092516 in osteoarthritis (OA)

Methods

Results

Conclusion