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Synovium is a sensitive tissue for mapping the negative effects of systemic iron overload in osteoarthritis:
Zhuangzhuang Jin1, He Zhang2, Lunhao Bai3
1Department of Emergence Medicine, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Background:
The prevention and treatment of osteoarthritis (OA) pose a major challenge in its research. The synovium is a critical tissue in the systematic treatment of OA. The present study aimed to investigate potential target genes and their correlation with iron overload in OA patients.
Methods:
The internal datasets for analysis included the microarray datasets GSE46750, GSE55457, and GSE56409, while the external datasets for validation included GSE12021 and GSE55235. The GSE176308 dataset was used to generate single-cell RNA sequencing profiles. To investigate the expression of the target genes in synovial samples, quantitative reverse transcription-PCR, western blotting, and immunohistochemical assay were conducted. ELISA was used to detect the levels of ferritin and Fe2+ in both serum and synovium.
Results:
JUN and ZFP36 were screened from the differentially expressed genes, and their mRNA were significantly reduced in the OA synovium compared to that in normal synovium. Subsequently, complex and dynamically evolving cellular components were observed in the OA synovium. The mRNA level of JUN and ZFP36 differed across various cell clusters of OA synovium and correlated with immune cell infiltration. Moreover, ferritin and Fe2+ were significantly increased in the serum and synovium of OA patients. Further, we found that JUN elevated and ZFP36 decreased at protein level.
Conclusions:
The synovium is a sensitive tissue for mapping the adverse effects of systemic iron overload in OA. JUN and ZFP36 represent potential target genes for attenuating iron overload during OA treatment. Some discrepancies between the transcription and protein levels of JUN suggest that post-transcriptional modifications may be implicated. Future studies should also focus on the roles of JUN and ZFP36 in inducing changes in cellular components in the synovium during OA pathogenesis.
Insights
Iron overload in osteoarthritis (OA) is linked to reduced JUN and ZFP36 gene expression in the synovium. These genes may be targets for treating OA and mitigating iron overload effects.
Area of Science:
- Biomedical research
- Molecular biology
- Osteoarthritis research
Background:
- Osteoarthritis (OA) presents significant challenges in prevention and treatment.
- The synovium plays a crucial role in OA pathogenesis and systemic treatment strategies.
- Investigating the link between iron overload and specific genes in OA is critical.
Purpose of the Study:
- To identify potential target genes associated with iron overload in osteoarthritis patients.
- To explore the correlation between gene expression and iron levels in synovial tissue.
- To understand the role of the synovium in the context of systemic iron overload in OA.
Main Methods:
- Utilized multiple microarray datasets (GSE46750, GSE55457, GSE56409, GSE12021, GSE55235) for differential gene expression analysis.
- Employed single-cell RNA sequencing (GSE176308) to analyze gene expression across synovial cell clusters.
- Quantified gene and protein expression (JUN, ZFP36) and iron markers (ferritin, Fe2+) using RT-PCR, Western blotting, immunohistochemistry, and ELISA.
Main Results:
- Identified JUN and ZFP36 as differentially expressed genes with significantly reduced mRNA levels in OA synovium compared to normal synovium.
- Observed distinct cellular components and immune cell infiltration in OA synovium, correlating with JUN and ZFP36 mRNA levels.
- Found significantly increased ferritin and Fe2+ levels in serum and synovium of OA patients, with elevated JUN protein and decreased ZFP36 protein.
Conclusions:
- The synovium is a key indicator of systemic iron overload's impact on OA.
- JUN and ZFP36 show potential as therapeutic targets for managing iron overload in OA treatment.
- Discrepancies in JUN transcription and protein levels suggest post-transcriptional regulation warrants further investigation.
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