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Identification of the Key Genes Involved in the Effect of Folic Acid on Endothelial Progenitor Cell Transcriptome of
Yi Lu1, Qianhong Yang2, Wei Hu1
1Department of Cardiology, Minhang Hospital, Fudan University, 170 Xin-Song Road, Shanghai 201199, China.
Insights
Folic acid (FA) influences endothelial progenitor cells (EPCs) in type 1 diabetes (T1D). This study identified key genes regulated by FA in T1D EPCs, offering insights into T1D pathogenesis and potential therapeutic targets.
Area of Science:
- Immunology
- Genetics
- Cell Biology
Background:
- Type 1 diabetes (T1D) is a prevalent childhood autoimmune disease.
- Endothelial progenitor cells (EPCs) and folic acid (FA) may play roles in T1D pathogenesis.
- Previous research suggests FA influences EPC function.
Purpose of the Study:
- To investigate the effects of FA on the transcriptome of EPCs from T1D patients.
- To identify key genes and biological pathways affected by FA treatment in T1D EPCs.
- To elucidate the role of FA in regulating EPCs in the context of T1D.
Main Methods:
- Isolation and treatment of EPCs from T1D patients with FA.
- Differential gene expression analysis to identify upregulated and downregulated genes.
- Bioinformatics analysis, including pathway enrichment and protein-protein interaction (PPI) network analysis.
Main Results:
- Identified 716 downregulated and 617 upregulated genes in FA-treated T1D EPCs.
- DEGs are involved in metabolic processes, cell proliferation, bone marrow development, cell adhesion, and growth factor response.
- Identified key regulatory genes, including 6 upregulated (e.g., POLR2A, BDNF) and 8 downregulated (e.g., SHC1, GRIN2B).
Conclusions:
- FA significantly alters the gene expression profile of EPCs in T1D patients.
- Specific genes identified may serve as crucial regulators in FA's effect on T1D EPCs.
- This study provides novel insights into FA's role in T1D, potentially informing therapeutic strategies.
Abstract:
Type 1 diabetes (T1D) is one of the most common autoimmune diseases in children. Previous studies have suggested that endothelial progenitor cells (EPCs) might be engaged in the regulating of the biological processes in T1D and folic acid (FA) might be engaged in regulating EPC function. The present study has identified 716 downregulated genes and 617 upregulated genes in T1D EPC cases after treated with FA. Bioinformatics analysis has shown that these DEGs were engaged in regulating metabolic processes, cell proliferation-related processes, bone marrow development, cell adhesion, platelet degranulation, and cellular response to growth factor stimulus. Furthermore, we have conducted and identified hub PPI networks. Importantly, we have identified 6 upregulated genes (POLR2A, BDNF, CDC27, LTN1, RAB1A, and CUL2) and 8 downregulated genes (SHC1, GRIN2B, TTN, GNAL, GNB2, PTK2, TF, and TLR9) as key regulators involved in the effect of FA on endothelial progenitor cell transcriptome of patients with T1D. We think that this study could provide novel information to understand the roles of FA in regulating EPCs of T1D patients.
