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LncRNA-GAS5 Inhibits Expression of miR 103 and Ameliorates the Articular Cartilage in Adjuvant-Induced Arthritis in
Hongwei Chen1,2, Chuan He1,2, Yan Liu2
1The Third Clinical Medical School, Yangtze University, Jingzhou, Hubei, China.
Abstract:
We explored whether long noncoding RNA growth arrest-specific transcript 5 (LncRNA-GAS5) small interfering RNA (siRNA) reduced cartilage destruction in obese mice with adjuvant-induced arthritis. We studied the effects of LncRNA-GAS5 siRNA on the polyarthritis index; hind paw swelling; and the serum levels of certain biochemicals, cytokines, and oxidative stress parameters. We measured the expression levels of matrix metalloproteinases (MMP)-13, NF-κB, fibroblast growth factor (FGF) 21, p38, Akt, and PI3K in cartilage via Western blotting and quantitative reverse transcription PCR. Long noncoding RNA-GAS5 siRNA reduced joint swelling; the serum levels of arthritis-associated biochemicals, cytokines, and oxidative stress markers; and cartilage MMP-13, NF-κB, FGF21, p38, Akt, and PI3K levels. Cartilage miR-103 expression was reduced. Histopathologically, LncRNA-GAS5 siRNA ameliorated the pathological changes of cartilage. Long noncoding RNA-GAS5 siRNA prevented cartilage destruction by inhibiting miR-103 expression.
Insights
Small interfering RNA targeting long noncoding RNA growth arrest-specific transcript 5 (LncRNA-GAS5 siRNA) effectively reduced cartilage destruction and inflammation in obese mice with adjuvant-induced arthritis.
Area of Science:
- Biochemistry
- Molecular Biology
- Immunology
Background:
- Obesity exacerbates arthritis, leading to significant cartilage destruction.
- Long noncoding RNAs (lncRNAs) play roles in inflammatory diseases.
- Growth arrest-specific transcript 5 (GAS5) is a lncRNA implicated in cellular processes.
Purpose of the Study:
- To investigate the therapeutic potential of LncRNA-GAS5 small interfering RNA (siRNA) in mitigating cartilage damage in a mouse model of obesity-induced arthritis.
- To elucidate the molecular mechanisms underlying the anti-arthritic effects of LncRNA-GAS5 siRNA.
Main Methods:
- Adjuvant-induced arthritis model in obese mice.
- Administration of LncRNA-GAS5 siRNA.
- Assessment of clinical arthritis scores (polyarthritis index, paw swelling).
- Measurement of serum biochemicals, cytokines, and oxidative stress markers.
- Analysis of cartilage gene and protein expression (MMP-13, NF-κB, FGF21, p38, Akt, PI3K, miR-103) via Western blotting and qRT-PCR.
- Histopathological evaluation of cartilage.
Main Results:
- LncRNA-GAS5 siRNA significantly reduced joint swelling and polyarthritis index.
- Serum levels of arthritis-associated biochemicals, cytokines, and oxidative stress markers were decreased.
- Expression of MMP-13, NF-κB, FGF21, p38, Akt, and PI3K in cartilage was downregulated.
- A reduction in cartilage miR-103 expression was observed.
- Histopathological analysis confirmed amelioration of cartilage damage.
Conclusions:
- LncRNA-GAS5 siRNA demonstrates a protective effect against cartilage destruction in obese mice with adjuvant-induced arthritis.
- The therapeutic mechanism involves the inhibition of miR-103 expression and downstream signaling pathways.
- Targeting LncRNA-GAS5 with siRNA presents a potential therapeutic strategy for inflammatory arthritis, particularly in obese individuals.
