RNA-seq reveals differential gene expression profiles of alveolar type II epithelial cells in young and aged mice lungs
Lung aging triggers the onset of various chronic lung diseases, with alveolar repair being a key focus for alleviating pulmonary conditions. The regeneration of epithelial structures, particularly the differentiation from type II alveolar epithelial (AT2) cells to type I alveolar epithelial (AT1) cells, serves as a prominent indicator of alveolar repair. Nonetheless, the precise role of aging in impeding alveolar regeneration and the underlying mechanism remain to be fully elucidated. To elucidate the mechanisms underlying AT2 cell functional decline during lung aging, we employed transcriptomic techniques to explicit the differences in gene expression between AT2 cells of young (3-month old) and old (24-month old) mouse lungs, and revealed correlation between inflammatory factors and genes regulating proliferation and differentiation. Physiological aging-induced chronic inflammation impairs AT2 cell functions, hindering tissue repair and promoting lung disease progression. This study offers novel insights into chronic inflammation's impact on stem cell-mediated alveolar regeneration. Overall design: To investigate the differential gene expression profile of AT2 cells during lung aging, we extracted primary cells from lung tissues of naturally aged C57/6J mice at 3 months and 24 months of age. Subsequently, flow cytometry was employed to sort CD45- CD31- CD326+ MHCII+ cells, which represent AT2 cells. The RNA-seq data of AT2 cells from these two age groups were analyzed to determine the differences in gene expression between young and old mouse lungs.