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An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
449
Increased long noncoding RNA LINK-A contributes to rheumatoid synovial inflammation and aggression
Jingnan Wang1, Chuyu Shen1, Ruiru Li1
1Department of Rheumatology and Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
JCI Insight
|December 8, 2021
Summary
Increased long noncoding RNA LINK-A expression in rheumatoid arthritis (RA) drives fibroblast-like synoviocyte (FLS) inflammation and aggression. Targeting LINK-A may offer a new therapeutic strategy for RA patients.
Area of Science:
- Rheumatology
- Molecular Biology
- Genetics
Background:
- Fibroblast-like synoviocytes (FLSs) are central to rheumatoid arthritis (RA) pathogenesis.
- The role of long noncoding RNAs (lncRNAs) in RA remains largely unexplored.
Purpose of the Study:
- Investigate the role of lncRNA LINK-A in RA.
- Determine the mechanisms by which LINK-A influences FLS function in RA.
Main Methods:
- Quantitative analysis of LINK-A expression in RA synovial tissues and FLSs.
- LINK-A knockdown experiments in RA FLSs.
- Mechanistic studies involving protein kinase signaling pathways and microRNA interactions.
Main Results:
- LINK-A expression is elevated in RA synovial tissues and FLSs, correlating with synovitis severity.
- LINK-A knockdown reduces RA FLS migration, invasion, and secretion of matrix metalloproteinases and inflammatory cytokines.
- LINK-A regulates FLS inflammation and invasion via tyrosine protein kinase 6/leucine-rich repeat kinase 2-mediated HIF-1α.
- LINK-A acts as a sponge for microRNA 1262, influencing FLS aggression.
Conclusions:
- Elevated LINK-A contributes to FLS-mediated inflammation and aggression in RA.
- LINK-A represents a potential therapeutic target for managing RA.
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