Islet β-cells physiological difference study of old and young mice based on single-cell transcriptomics

Body aging is a universal biological process. With aging, cells undergo a series of physiological changes. The main feature is cell proliferation decline, although the cells still have normal functions. Pancreatic β-cells are no exception. However, the physiological senescence of β-cells, and the resulting function and transcriptome changes have rarely attracted attention. The specific senescence phenotype of β-cells remains unknown.

Pancreatic samples from three female C57BL/6 mice with aged 2.5 months (young) mice and 20 months (old) were digested to a single-cell suspension and analyzed, with 10× Genomics single-cell ribonucleic acid sequencing, β-cells were determined by biosynthesis analysis, and differences between old and young mice were identified.

A total of 47 differential genes with significant and statistical significance were screened in β-cells (fold change >1.5, P < 0.05). In old mice, 27 genes were upregulated and 20 genes were downregulated. Genes Mt1, Mt2, Pyy, Gcg and Pnlip, and mitochondrial genes mt-Nd1, mt-Nd3, mt-Co1, mt-Co2 and mt-Co3 were found to be involved in cellular senescence. Transcription factors Jund and Fos were important regulators of senescence.

An overall difference was found between the pancreatic β-cells of old and young mice. Transcription factors facilitate transitions between pancreatic β-cells. These findings are worthy of deep exploration, and provide new resources and directions for the research of pancreatic aging in mice.