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Capg enhances proliferation, adipogenesis, and inflammatory response in preadipocytes: insights from bioinformatics
Luyao Zhang1,2, Botao Sang3, Sainan Li1,2
1National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Background:
Various associations between adipose tissue and atherosclerosis (AS) have been revealed. This study aims to identify biomarkers in the epididymal adipose tissue of AS mice and to explore their effects on adipose tissue inflammation and adipogenesis.
Methods:
The gene expression profiles of epididymal adipose tissue (GSE57659 and GSE76812) were downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEG) screened by Limma R package and genes searched by weighted gene correlation network analysis (WGCNA) were performed to classify common genes associated with AS. The Protein-Protein interaction (PPI) network was constructed by Cytoscape software, and hub genes were eventually determined by the Cytohubba plugin. Finally, one of these hub genes was selected. The cell proliferation ability was assessed using the CCK8 assay. Oil Red O staining and Western blot were employed to evaluate the lipid content in adipocytes. The extent of the inflammatory response in adipocytes was determined by Enzyme-Linked Immunosorbent Assay (ELISA).
Results:
A total of 125 DEGs were identified between the control group and the atherosclerosis group. Among these, 34 genes were selected based on two key modules identified through WGCNA. Subsequently, five key nodes were identified, namely Capg, Timp1, Lgals3, Agt, and Mmp9. Capg was selected as the primary gene of interest for further investigation. Following the transfection of 3T3-L1 cells with lentivirus, Capg was overexpressed. Capping actin protein, gelsolin like (CAPG) significantly enhanced preadipocyte proliferation, as demonstrated by CCK-8 and upregulated expression of the Cyclin D1. Furthermore, Oil Red O staining revealed a marked elevation in intracellular lipid accumulation upon CAPG overexpression. Western blot analysis showed increased protein levels of PPAR γ and adiponectin. Furthermore, CAPG in 3T3-L1 cells resulted in a marked upregulation of IL-6 and MCP-1.
Conclusion:
CAPG promotes the proliferation and differentiation of adipocyte precursor cells. Additionally, CAPG enhances the inflammatory response in adipocytes, potentially serving as a key molecule mediating obesity-related atherosclerosis.
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