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Updated: Aug 9, 2025

Tissue Collection and RNA Extraction from the Human Osteoarthritic Knee Joint
Published on: July 22, 2021
RNA-Seq Reveals the mRNAs, miRNAs, and lncRNAs Expression Profile of Knee Joint Synovial Tissue in Osteoarthritis
Linghui Qiao1, Jun Gu1, Yingjie Ni1
1Wuxi Xishan People's Hospital (Wuxi Branch of Zhongda Hospital Affiliated to Southeast University), Wuxi 214000, China.
Abstract:
Osteoarthritis (OA) is a chronic disease common in the elderly population and imposes significant health and economic burden. Total joint replacement is the only currently available treatment but does not prevent cartilage degeneration. The molecular mechanism of OA, especially the role of inflammation in disease progression, is incompletely understood. We collected knee joint synovial tissue samples of eight OA patients and two patients with popliteal cysts (controls), measured the expression levels of lncRNAs, miRNAs, and mRNAs in these tissues by RNA-seq, and identified differentially expressed genes (DEGs) and key pathways. In the OA group, 343 mRNAs, 270 lncRNAs, and 247 miRNAs were significantly upregulated, and 232 mRNAs, 109 lncRNAs, and 157 miRNAs were significantly downregulated. mRNAs potentially targeted by lncRNAs were predicted. Nineteen overlapped miRNAs were screened based on our sample data and GSE 143514 data. Pathway enrichment and functional annotation analyses showed that the inflammation-related transcripts CHST11, ALDH1A2, TREM1, IL-1β, IL-8, CCL5, LIF, miR-146a-5p, miR-335-5p, lncRNA GAS5, LINC02288, and LOC101928134 were differentially expressed. In this study, inflammation-related DEGs and non-coding RNAs were identified in synovial samples, suggesting that competing endogenous RNAs have a role in OA. TREM1, LIF, miR146-5a, and GAS5 were identified to be OA-related genes and potential regulatory pathways. This research helps elucidate the pathogenesis of OA and identify novel therapeutic targets for this disorder.
Insights
This study identified key inflammation-related genes and non-coding RNAs in osteoarthritis (OA) synovial tissue. These findings suggest a role for competing endogenous RNAs in OA pathogenesis and offer potential new therapeutic targets for this chronic joint disease.
Area of Science:
- Molecular biology
- Genomics
- Rheumatology
Background:
- Osteoarthritis (OA) is a prevalent degenerative joint disease in the elderly, causing significant health and economic burdens.
- Current treatments like total joint replacement do not halt cartilage degeneration, and the molecular mechanisms, particularly inflammation's role, remain unclear.
Purpose of the Study:
- To investigate the molecular mechanisms of osteoarthritis (OA) by analyzing gene and non-coding RNA expression in synovial tissues.
- To identify differentially expressed genes (DEGs) and key pathways involved in OA pathogenesis, focusing on inflammation.
Main Methods:
- RNA sequencing (RNA-seq) was performed on knee joint synovial tissue samples from OA patients and controls.
- Analysis included identification of differentially expressed mRNAs, lncRNAs, and miRNAs, prediction of lncRNA-mRNA interactions, and screening of overlapping miRNAs.
- Pathway enrichment and functional annotation were conducted to identify key biological processes.
Main Results:
- Significant upregulation and downregulation of numerous mRNAs, lncRNAs, and miRNAs were observed in OA samples compared to controls.
- Key inflammation-related transcripts including CHST11, TREM1, IL-1β, IL-8, miR-146a-5p, and lncRNA GAS5 were identified as differentially expressed.
- Specific genes like TREM1, LIF, miR146-5a, and GAS5 were highlighted as potentially crucial in OA development and regulation.
Conclusions:
- This study identified inflammation-related differentially expressed genes and non-coding RNAs in OA synovial tissues.
- The findings suggest that competing endogenous RNA networks play a role in the pathogenesis of osteoarthritis.
- The identified genes and pathways, such as TREM1, LIF, miR146-5a, and GAS5, represent potential novel therapeutic targets for OA treatment.
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