J Diabetes Investig. 2021 May 18. doi: 10.1111/jdi.13579. Online ahead of print.
ABSTRACT
BACKGROUND: 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 cell 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.
MATERIALS AND METHODS: 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×genomic single-cell RNA sequencing (scRNA-seq), β cells were determined by biosynthesis analysis, and differences between old and young mice were identified.
RESULTS: Forty-seven 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 up-regulated and 20 genes were down-regulated. 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.
CONCLUSIONS: 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.
PMID:34003589 | DOI:10.1111/jdi.13579
