<p>Downregulation of microRNA-23b-3p alleviates IL-1β-induced injury in chondrogenic CHON-001 cells</p>

Abstract

Background: Osteoarthritis (OA) is a common joint disease, which is characterized by degradation of articular cartilage. Evidence indicated that miR-23b-3p was upregulated in cartilage tissues of a patient with OA. However, the mechanism by which miR-23b-3p regulates the occurrence and development of OA remains unclear. Thus, this study aimed to investigate the role of miR-23b-3p in the progression of OA. Methods: In this study, qRT-PCR was used to measure the expression of miR-23b-3p in OA tissue samples and normal controls, respectively. Western blotting assay was performed to detect the levels of collagen II, aggrecan, Bax and active caspase 3 in CHON-001 cells. In addition, the dual-luciferase reporter system assay was used to detect the interaction between miR-23b-3p and COL11A2 in OA. Results: The levels of miR-23b-3p were upregulated, while the expressions of collagen II and aggrecan were decreased in OA tissues and in IL-1β-treated CHON-001 cells. In addition, IL-1β significantly induced apoptosis of CHON-001 cells via increasing the levels of Bax and active caspase 3. However, downregulation of miR-23b-3p markedly inhibited IL-1β-induced apoptosis in CHON-001 cells via increasing the collagen II and aggrecan levels and decreasing Bax and active caspase 3 expressions. Meanwhile, dual-luciferase assay showed that COL11A2 was the direct target of miR-23b-3p in CHON-001 cells. Overexpression of miR-23b-3p markedly decreased the level of COL11A2 in cells. Moreover, downregulation of miR-23b-3p alleviated synovitis/cartilage destruction and reduced Osteoarthritis Research Society International scores and subchondral bone thickness in vivo. Conclusion: Downregulation of miR-23b-3p could alleviate the progression of OA through upregulating COL11A2 in vivo and in vitro. Therefore, downregulation of miR-23b-3p might be a potential therapeutic strategy for the treatment of OA.

The trans-omics landscape of COVID-19

“…Posttranscription of inflammation-related mRNAs is mainly regulated by RNA-binding proteins (RBPs) and microRNAs. Interestingly, RBPs (HNRNPD, ZFP36, ZC3H12A, ILF3, ZNF692, FXR1, ELAVL1, and BRF1/2) and microRNAs (miR-181a-5p, miR-181a-2-3p, miR-10a-5p, miR-23b-3p), which might involved in the degradation and destabilization of inflammatory cytokines [45][46][47][48] , were highly expressed in asymptomatic patients but lowly expressed in critical patients (Fig. 4g, h).…”

Potential of miR-25-3p in protection of chondrocytes: emphasis on osteoarthritis

“…An investigation with larger sample sizes are needed to provide a deeper insight regarding which pathways miR-25-3p modulates to affect the proliferation and apoptosis of OA chondrocytes. More and more methods have been shown to be effective in treating OA [33][34][35]. Therefore, it is still vital to explore new potential treatment strategies for OA progression.…”

CircRNA circ‐IQGAP1 Knockdown Alleviates Interleukin‐1β‐Induced Osteoarthritis Progression via Targeting miR‐671‐5p/TCF4

“…Thus, we hypothesized that circ‐IQGAP1 might target TCF4 by competitively binding tomiR‐671‐5p, regulating IL‐1β‐caused damage in chondrocytes. In this research, we established an in vitro model of OA using IL‐1β‐challenged chondrocytes (CHON‐001) as previously reported 27–29 . The purpose of this study was: (i) to investigate the function of circ‐IQGAP1 on IL‐1β‐caused chondrocyte apoptosis, inflammatory injury, and extracellular matrix degradation; (ii) to analyze the regulatory network of circ‐IQGAP1/miR‐671‐5p/TCF4 in chondrocytes; and (iii) to explore whether circ‐IQGAP1 regulated the miR‐671‐5p/TCF4 axis to modulate chondrocyte apoptosis, inflammatory injury, and extracellular matrix degradation.…”