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ITGB1 alleviates osteoarthritis by inhibiting cartilage inflammation and apoptosis via activating cAMP pathway
Lifeng Xie1, Zhengnan Li2, Zhijun Chen1
1Department of Orthopedics, Second Affiliated Hospital of Nanchang University, No.1 MinDe Road, Donghu District, Nanchang City, 330000, Jiangxi Province, China.
Objective:
We aimed to screen novel biomarkers for osteoarthritis (OA) using bioinformatic methods and explore its regulatory mechanism in OA development.
Methods:
Differentially expressed genes were screened out from GSE98918 and GSE82107 datasets. Protein-protein interaction network and enrichment analysis were employed to search for hub gene and regulatory pathway. Hematoxylin-eosin, Safranin O-Fast green staining, and immunohistochemistry were performed to assess pathological damage. TNF-α, IL-1β, and IL-6 concentrations were determined by enzyme-linked immunosorbent assay. Real-time quantitative PCR was applied to verify expression of hub genes in OA model. The expression of key protein and pathway proteins was determined by western blot. Furthermore, Cell Counting Kit-8 and flow cytometry were conducted to explore the role of hub gene in chondrocytes.
Results:
We identified 6 hub genes of OA, including ITGB1, COL5A1, COL1A1, THBS2, LAMA1, and COL12A1, with high prediction value. ITGB1 was screened as a pivotal regulator of OA and cAMP pathway was selected as the key regulatory pathway. ITGB1 was down-regulated in OA model. ITGB1 overexpression attenuated pathological damage and apoptosis in OA rats with the reduced levels of TNF-α, IL-1β and IL-6. ITGB1 overexpression activated cAMP pathway in vivo and vitro models. In vitro model, ITGB1 overexpression promoted cell viability, while inhibited apoptosis. ITGB1 overexpression also caused a decrease of TNF-α, IL-1β, and IL-6 concentrations. cAMP pathway inhibitor reversed the positive effect of ITGB1 on OA cell model.
Conclusion:
ITGB1 is a novel biomarker for OA, which inhibits OA development by activating the cAMP pathway.
Insights
Integrin beta 1 (ITGB1) is a novel osteoarthritis biomarker. Overexpressing ITGB1 in osteoarthritis models reduced inflammation and apoptosis by activating the cAMP pathway.
Area of Science:
- Biomarker discovery
- Molecular mechanisms of osteoarthritis
- Integrin signaling
Background:
- Osteoarthritis (OA) is a degenerative joint disease with limited effective biomarkers.
- Understanding the molecular pathways involved in OA pathogenesis is crucial for developing new treatments.
Purpose of the Study:
- To identify novel biomarkers for osteoarthritis using bioinformatics.
- To elucidate the regulatory mechanisms of identified biomarkers in OA development.
Main Methods:
- Bioinformatic analysis of gene expression datasets (GSE98918, GSE82107).
- Protein-protein interaction network and enrichment analysis to identify hub genes and pathways.
- In vivo and in vitro OA models to assess pathological damage, apoptosis, and inflammatory markers (TNF-α, IL-1β, IL-6).
- Real-time quantitative PCR, western blot, Cell Counting Kit-8, and flow cytometry were used to validate gene and protein expression and cellular functions.
Main Results:
- Six hub genes were identified, with ITGB1 selected as a pivotal regulator.
- ITGB1 expression was downregulated in OA models.
- ITGB1 overexpression attenuated OA pathology, reduced inflammation and apoptosis in rats, and promoted chondrocyte viability.
- ITGB1 activated the cAMP pathway, and its inhibition reversed the protective effects.
Conclusions:
- Integrin beta 1 (ITGB1) is a novel and promising biomarker for osteoarthritis.
- ITGB1 exerts protective effects against OA development by activating the cAMP pathway, suggesting therapeutic potential.
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