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Capg enhances proliferation, adipogenesis, and inflammatory response in preadipocytes: insights from bioinformatics analysis and functional validation

cardiology
metabolic-sciences

Abstract

Background: Various associations between adipose tissue and atherosclerosis (AS) have been identified. This study aims to identify biomarkers in the epididymal adipose tissue of AS mice and explore their roles in adipose tissue inflammation and adipogenesis.

Methods: Gene expression profiles of epididymal adipose tissue (GSE57659 and GSE76812) were obtained from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified using the Limma R package, and weighted gene correlation network analysis (WGCNA) was used to identify gene modules associated with AS. Common genes were selected for further analysis. A proteinā€“protein interaction (PPI) network was constructed using Cytoscape, and hub genes were identified with the CytoHubba plugin. One hub gene, Capg, was selected for functional validation. Cell proliferation was assessed using the CCK-8 assay. Lipid accumulation in adipocytes was evaluated by Oil Red O staining and Western blot. Inflammatory responses were measured using ELISA.

Results: A total of 125 DEGs were identified between the control and AS groups. Of these, 34 genes were associated with two key WGCNA modules. Five hub genes were identified: Capg, Timp1, Lgals3, Agt, and Mmp9. Capg was selected for further study. Overexpression of Capg in 3T3-L1 cells via lentiviral transfection significantly enhanced preadipocyte proliferation, as shown by the CCK-8 assay and increased Cyclin D1 expression. Oil Red O staining revealed increased intracellular lipid accumulation, and Western blot analysis showed elevated levels of PPARĪ³ and Adiponectin. Additionally, Capg overexpression led to increased secretion of IL-6 and MCP-1, indicating an enhanced inflammatory response.


Conclusion: CAPG promotes the proliferation and differentiation of adipocyte precursor cells and enhances inflammatory responses in adipocytes. These findings suggest that CAPG may be a key molecule linking adipose tissue dysfunction to obesity-related atherosclerosis.
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