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Published on: February 20, 2019
Elucidating the role of LGALS3BP in coronary atherosclerosis: integrating bioinformatics and machine learning for
Suzhen Zhao1, Chuanxin Zhao1, Linlin Wang1
1Dongying People's Hospital (Dongying Hospital of Shandong Provincial Hospital Group), Dongying, Shandong, 257091, PR China.
Insights
LGALS3BP is linked to atherosclerosis (AS) inflammation. Higher LGALS3BP expression correlates with increased immune cell infiltration, suggesting its potential as a biomarker for AS diagnosis and monitoring.
Area of Science:
- Immunology
- Molecular Biology
- Vascular Biology
Background:
- Atherosclerosis (AS) is a chronic inflammatory vascular disease.
- LGALS3BP is a molecule involved in physiological and pathological processes.
Purpose of the Study:
- To investigate the role of LGALS3BP in atherosclerosis.
- To identify LGALS3BP as a potential biomarker for AS.
Main Methods:
- Integrative analysis of gene expression datasets (GSE43292, GSE9820) and immune gene sets.
- Utilized Lasso regression and SVM-RFE for gene selection.
- Employed CIBERSORT and ESTIMATE algorithms to assess immune cell infiltration and LGALS3BP expression correlation.
Main Results:
- Identified 13 hub genes associated with LGALS3BP.
- LGALS3BP expression positively correlates with various immune cells including T cells and NK cells.
- LGALS3BP expression is negatively associated with M0 macrophages and eosinophils.
Conclusions:
- LGALS3BP is implicated in immune responses within atherosclerosis.
- LGALS3BP shows potential as a novel biomarker for AS diagnosis and monitoring.
- Targeting LGALS3BP pathways may offer therapeutic strategies for AS.
Background:
Atherosclerosis (AS) is increasingly recognized as a chronic inflammatory disease that significantly impacts vascular health and contributes to cardiovascular disorders. LGALS3BP, a well-studied molecule, plays key roles in various physiological and pathological processes.
Methods:
We identified LGALS3BP as a central focus through integrative analysis of DEGs across multiple datasets (GSE43292 and GSE9820) from the GEO database, combined with immune-related gene sets from the ImmPort database. Advanced analytical techniques, including Lasso regression and SVM-RFE, were used to refine gene selection. GSEA and GSVA revealed significant enrichment in immune-related pathways. The relationship between LGALS3BP expression and immune processes was explored using CIBERSORT and ESTIMATE algorithms, which indicated a positive association between higher LGALS3BP expression and increased immune cell infiltration.
Results:
Among the 10 DEGs associated with LGALS3BP, 13 hub genes were identified via LASSO and SVM-RFE analyses. Functional assays highlighted LGALS3BP's involvement in viral defense, cytokine production, and immune cascades. Increased expression of LGALS3BP was positively correlated with activated dendritic cells, NK cells, memory CD4 T cells, naïve CD4 T cells, CD8 T cells, follicular helper T cells, gamma delta T cells, and regulatory T cells (Tregs), while negatively associated with resting mast cells, M0 macrophages, and eosinophils.
Conclusions:
Our research elucidates the complex relationship between LGALS3BP and AS, positioning it as a potential novel biomarker for diagnosis and disease monitoring. These findings lay the groundwork for future studies and suggest that targeting LGALS3BP-related pathways could enhance our understanding of AS.
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