AI Article Synopsis
- Type 1 diabetes (T1D) is linked to poor islet mass and survival rates, prompting a study to identify genes and pathways that could enhance islet longevity during culture.
- The researchers utilized bioinformatics by analyzing gene expression data from a specific microarray, examining differently methylated genes, and conducting gene ontology and pathway enrichment analyses.
- Their findings highlighted several key genes (FN1, MKI67, IGF1, MAPK14, COL1A1) associated with important signaling pathways (TGF-beta, MAPK, VEGF) that may play a role in improving islet survival and culture conditions.
Article Abstract
Type 1 diabetes (T1D) is characterized by non-ideal mass and low survival rate of islets. Therefore, it is necessary to find intrinsic factors that prolong the survival of islets. This study aimed to track out hub genes and pathways in the process of islet culture by bioinformatic analysis. We downloaded the gene expression microarray of GSE42591 from the Gene Expression Omnibus (GEO). Aberrant Differentially methylated genes (DMGs) were obtained using the GEO2R tool. Gene ontology (GO) analysis and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway enrichment analyses were performed on selected genes by using the Database for Annotation Visualization and Integrated Discovery (DAVID). A protein-protein interaction (PPI) network was constructed with the Retrieval of Interacting Genes (STRING) and visualized in Cytoscape 3.7.2. A total of 434 genes were overexpressed and 114 genes underexpressed in fresh to cultured 4 h tissue. KEGG pathway enrichment analyses revealed the TGF-beta signaling pathway, MAPK signaling pathway, or VEGF signaling pathway. The genes FN1, MKI67, IGF1, MAPK14, COL1A1 might be involved in islet culture. In general, this work scrutinized islet culture-relevant knowledge and provided insight into the regulation and mediation of islet survival.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7868784 | PMC |
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