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Updated: Feb 15, 2026
Synovial Fluid Analysis to Identify Osteoarthritis
Published on: October 20, 2022
LINC00312 affects the progression of osteoarthritis by targeting miR-331-3p/DUSP5 axis
Dengke Zhao1, Yiming Zhao1, Yuxiang He1
1Department of Orthopedics, Qilu Hospital of Shandong University, 107 Wenhua West Road, Jinan, Shandong, 250012, China.
Background:
As a chronic degenerative disease, osteoarthritis (OA) manifests through articular cartilage breakdown and ongoing inflammatory processes in joints. Recently, long non-coding RNAs (lncRNAs) have been participated in pathological process of OA through epigenetic regulation and molecular signaling axis.
Aim:
This study aimed to verify whether LINC00312 regulates DUSP5 expression by adsorbing miR-331-3p as a competitive endogenous RNA (ceRNA) in OA, thereby exerting a cartilage-protective effect.
Methods:
Expressions of LINC00312, miR-331-3p, and dual-specific protein phosphatase 5 (DUSP5) in patient tissues and chondrocytes were detected by reverse transcription-quantitative PCR (RT-qPCR). An in vitro OA model was constructed by stimulating chondrocytes with IL-1β. Cell viability and apoptosis were assessed via cell counting kit-8 (CCK-8) assays and flow cytometry. The levels of chondrogenic-related genes and proinflammatory factors were detected by RT-qPCR and enzyme-linked immunosorbent assay (ELISA). Interaction of miR-331-3p with LINC00312 and DUSP5 was detected via dual luciferase assays and RIP assays. Correlation between LINC00312, miR-331-3p, and DUSP5 in patients with OA was analyzed using Pearson correlation analysis.
Results:
In OA patients' cartilage tissue and IL-1β-induced OA models, LINC00312 and DUSP5 expression decreased while miR-331- 3p expression increased. Overexpression of LINC00312 ameliorated cell injury induced by IL-1β stimulation, enhanced cell viability, and reduced apoptosis, MMP13, ADAMTS5, IL-6, and IL-8 levels. miR-331-3p negatively correlated with LINC00312, and upregulation of miR-331-3p reversed the protective effect of LINC00312. Additionally, DUSP5 was a direct target of miR-331-3p, and LINC00312 and miR-331-3p jointly regulated DUSP5 expression.
Conclusions:
LINC00312 alleviates IL-1β-induced chondrocyte inflammation and apoptosis by acting as a ceRNA to regulate the miR-331-3p/DUSP5 axis. This suggests that LINC00312 may serve as a novel therapeutic target for OA.
Insights
Long non-coding RNA LINC00312 protects against osteoarthritis by regulating the miR-331-3p/DUSP5 axis, reducing chondrocyte inflammation and apoptosis. This finding highlights LINC00312 as a potential therapeutic target for osteoarthritis.
Area of Science:
- Molecular Biology
- Genetics
- Biochemistry
Background:
- Osteoarthritis (OA) is a chronic degenerative joint disease characterized by cartilage breakdown and inflammation.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their role in OA pathogenesis via epigenetic regulation and molecular signaling.
Purpose of the Study:
- To investigate if LINC00312 acts as a competitive endogenous RNA (ceRNA) by sponging miR-331-3p to regulate dual-specific protein phosphatase 5 (DUSP5) expression.
- To determine the cartilage-protective effects of the LINC00312/miR-331-3p/DUSP5 axis in osteoarthritis.
Main Methods:
- Quantitative PCR (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA) were used to measure gene and protein expression.
- In vitro osteoarthritis models were established using IL-1β-stimulated chondrocytes.
- Cell viability, apoptosis, and inflammatory markers were assessed using CCK-8 assays, flow cytometry, and ELISA.
- Dual luciferase and RNA immunoprecipitation (RIP) assays confirmed molecular interactions.
- Pearson correlation analysis assessed relationships in patient samples.
Main Results:
- LINC00312 and DUSP5 expression were decreased, while miR-331-3p expression was increased in OA tissues and models.
- Overexpression of LINC00312 reduced IL-1β-induced chondrocyte injury, apoptosis, and levels of MMP13, ADAMTS5, IL-6, and IL-8.
- miR-331-3p negatively correlated with LINC00312, and its upregulation reversed LINC00312's protective effects.
- DUSP5 was identified as a direct target of miR-331-3p, with LINC00312 and miR-331-3p jointly regulating DUSP5.
Conclusions:
- LINC00312 alleviates IL-1β-induced chondrocyte inflammation and apoptosis by functioning as a ceRNA to modulate the miR-331-3p/DUSP5 pathway.
- LINC00312 demonstrates potential as a novel therapeutic target for osteoarthritis management.
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