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LINC02288 promotes chondrocyte apoptosis and inflammation through miR-374a-3p targeting RTN3
1Joint Surgery and Sports Medicine Department, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.
Background:
Dysregulation of long non-coding RNAs (lncRNAs) is related to the occurrence of osteoarthritis (OA). In the present study, we explored the role of LINC02288 and its regulatory mechanism in OA development.
Methods:
GSE113825 was obtained from Gene Expression Omnibus (GEO) database and analyzed to identify the differentially expressed lncRNAs in OA. Gene enrichment analyses and Kyoto Encyclopedia of Genes and Genomes biological process analysis were performed through Metascape (http://metascape.org/gp). The interactions among LINC02288, miR-374a-3p and RTN3 were determined using RNA immunoprecipitation (RIP) assays and dual luciferase reporter assays. Chondrocyte apoptosis was examined using flow cytometry. Western blot assays were conducted to assess the pro-apoptotic and anti-apoptotic markers.
Results:
We identified a total of 4,491 differentially expressed lncRNAs. We focused on LINC02288 as the top-ranked up-regulated lncRNA in OA as indicated by a significant p-value. LINC02288 was significantly up-regulated, which was further verified by a real-time polymerase chain reaction. Down-regulation of LINC02288 significantly reduced the apoptosis of OA chondrocytes induced by interleukin-1β and the production of pro-inflammatory cytokines. These effects were further verified in an OA rat model. An RIP assay and dual luciferase assay further confirmed that LINC02288 served as a sponge of miR-374a-3p. Moreover, the overexpression of RTN3 could partially reverse the effects of LINC02288 knockdown, mediating inhibitory effects on chondrocyte apoptosis and the inflammatory response. Down-regulation of LINC02288 alleviated OA development in an in vivo OA animal model.
Conclusions:
Our findings indicate that LINC02288 contributes to OA progression by targeting the miR-374a-3p/RTN3 axis, which might provide a promising molecular therapy strategy for OA.
Insights
Long non-coding RNA LINC02288 promotes osteoarthritis (OA) by regulating the miR-374a-3p/RTN3 pathway. Down-regulating LINC02288 alleviates OA progression and chondrocyte apoptosis.
Area of Science:
- Molecular Biology
- Genetics
- Biochemistry
Background:
- Long non-coding RNAs (lncRNAs) are implicated in osteoarthritis (OA) pathogenesis.
- The specific role and regulatory mechanisms of LINC02288 in OA remain largely unexplored.
Purpose of the Study:
- To investigate the function of LINC02288 in osteoarthritis.
- To elucidate the molecular mechanism underlying LINC02288's role in OA development.
Main Methods:
- Differential expression analysis of lncRNAs in OA using Gene Expression Omnibus (GEO) data.
- Validation of LINC02288 expression via real-time PCR.
- Investigation of LINC02288's interaction with miR-374a-3p and RTN3 using RIP and dual luciferase assays.
- Assessment of chondrocyte apoptosis and inflammatory cytokine production.
- Evaluation of LINC02288's effect in an OA rat model.
Main Results:
- LINC02288 was identified as a significantly up-regulated lncRNA in OA.
- Down-regulation of LINC02288 reduced OA chondrocyte apoptosis and pro-inflammatory cytokine production.
- LINC02288 acts as a molecular sponge for miR-374a-3p.
- RTN3 overexpression partially reversed the effects of LINC02288 knockdown.
- LINC02288 down-regulation alleviated OA progression in a rat model.
Conclusions:
- LINC02288 promotes OA progression through the miR-374a-3p/RTN3 axis.
- LINC02288 represents a potential therapeutic target for osteoarthritis.
