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

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.

Huang Z ，Ma W ，Xiao J ，Dai X ，Ling W ... -  《-》

Circular RNA-9119 protects IL-1β-treated chondrocytes from apoptosis in an osteoarthritis cell model by intercepting the microRNA-26a/PTEN axis.

Osteoarthritis (OA) is a common degenerative joint disease characterized by cartilage degeneration and joint inflammation. As its pathogenesis remains unclear, there are no effective treatments established. Circular RNA (circRNA), microRNA (miRNA), and other noncoding RNAs participate in OA development; however, the effects and mechanisms of circRNA and miRNA in OA remain unknown. Cartilage miRNA was examined in patients with and without OA. CircRNA-9119 and phosphatase and tensin homolog (PTEN) expression decreased in OA-affected cartilage and interleukin (IL)-1β-induced chondrocytes, and miR-26a expression significantly decreased in normal cells and tissues. CircRNA-9119 overexpression restored chondrocyte growth, whereas IL-1β treatment impaired chondrocyte growth. Annexin V-FITC & PI flow cytometry and Bcl-2/Bax ratio measurement indicated that the apoptosis of IL-1β-treated articular chondrocytes was decreased by circRNA-9119 upregulation. Bioinformatic prediction and the dual-luciferase reporter assay indicated that circRNA-9119 served as a miR-26a sponge and that miR-26a targeted the 3'-UTR of PTEN. Transfection of chondrocytes with a circRNA-9119-overexpressing vector revealed downregulation of miR-26a expression. Furthermore, circRNA-9119 overexpression induced PTEN expression. In addition, a miR-26a mimic induced IL-1β-induced chondrocyte apoptosis, and circRNA-9119 overexpression inhibited IL-1β-induced chondrocyte apoptosis. CircRNA-9119 is an important regulator of IL-1β-treated chondrocytes through the miR-26a/PTEN axis, possibly contributing to OA development.

Chen C ，Yin P ，Hu S ，Sun X ，Li B ... -  《-》

Circ_0116061 regulated the proliferation, apoptosis, and inflammation of osteoarthritis chondrocytes through regulating the miR-200b-3p/SMURF2 axis.

Zheng W ，Hou G ，Li Y 《Journal of Orthopaedic Surgery and Research》

Low expression of CircRNA HIPK3 promotes osteoarthritis chondrocyte apoptosis by serving as a sponge of miR-124 to regulate SOX8.

Wu Q ，Yuan ZH ，Ma XB ，Tang XH ... -  《-》

MiR-337-3p promotes chondrocytes proliferation and inhibits apoptosis by regulating PTEN/AKT axis in osteoarthritis.

Osteoarthritis (OA) is a degenerative disease of articular cartilage and its main pathological feature is cartilage destruction, but its specific pathogenesis is still debatable. The aim of this study was to explore the role of miR-337-3p in OA pathogenesis. The expression of miR-337-3p and PTEN in osteoarthritic cartilage tissues was detected using quantitative real time PCR and western blot, respectively. The regulation of miR-337-3p on PTEN was examined by luciferase reporter gene assays. The manipulation of miR-337-3p and PTEN was mediated by siRNA interference technology. The cell viability was analyzed by MTT assays. MiR-337-3p expression was significantly down-regulated in osteoarthritic cartilage tissues compared with normal cartilage tissues. Further studies confirmed that miR-337-3p overexpression evidently promoted the proliferation and inhibited the apoptosis of OA chondrocytes. PTEN expression was significantly up-regulated in osteoarthritic cartilage tissues and was negatively regulated by miR-337-3p in chondrocytes. PTEN silencing could improve the proliferation of OA chondrocytes and increased pAKT protein expression in OA chondrocytes. MiR-337-3p regulated OA chondrocytes proliferation through PTEN/AKT axis and thus involved in OA.

Huang Z ，Zhang N ，Ma W ，Dai X ，Liu J ... -  《-》