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The following is a summary of “Identification of a pancreatic stellate cell gene signature and lncRNA interactions associated with type 2 diabetes progression,” published in the January 2025 issue of Endocrinology by Qiu et al.
Type 2 diabetes (T2D) had emerged as a significant global health threat, yet its precise causes and mechanisms remained unclear.
Researchers conducted a retrospective study to identify gene expression patterns specific to T2D pancreatic islet cells and explore the potential role of pancreatic stellate cells (PSCs) in T2D progression through regulatory networks involving lncRNA-mRNA interactions.
They screened upregulated genes in T2D pancreatic islet samples using bulk sequencing (bulkseq) datasets and mapped the gene expression profiles to 3 T2D single-cell RNA sequencing (scRNAseq) datasets, T2D-specific gene features were validated using an additional T2D scRNAseq dataset, a T1D scRNAseq dataset, and a T2D bulkseq dataset. Regulatory networks were explored by analyzing potential lncRNA-mRNA interactions within T2D peripheral blood mononuclear cell (PBMC) bulkseq data.
The results showed a gene panel comprising COL1A2, VCAN, and SULF1 was consistently upregulated in T2D pancreatic islet samples. The expression of this panel was strongly linked to PSC activation, forming a T2D-specific signature (COL1A2hi /VCANhi /SULF1hi PSCs) not observed in Type 1 diabetes (T1D) samples. Additionally, 6 long non-coding RNAs (lncRNAs) were identified that may interact with the COL1A2hi /VCANhi /SULF1hi PSCs, forming a lncRNA-mRNA network potentially involved in modulating immune 7and reshaping the immune microenvironment in T2D.
Investigators concluded a potential immune-regulatory role for PSCs in T2D, identifying PSC-related lncRNA-mRNA networks as promising novel therapeutic targets for T2D treatment, thus providing valuable insights into PSCs as key modulators in T2D progression.
Source: frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2024.1532609/full