Analysis of gene expression modulated by autophagy during bleomycin induced lung injury from mouse lung alveolar progenitor cells

Autophagy is a cellular catabolic process that supports metabolism in response to stress. To identify gene expression that are modulated by autophagy in AT2 cells during BLM-induced lung injury, RNA-seq profiling were carried out with AT2 cells from Atg5f/f mice treated with PBS (AT2-PBS), Nkx2.1Cre; Atg5f/f mice treated with PBS (Atg5-/- AT2-PBS), Atg5f/f mice treated with BLM (AT2-BLM), and Nkx2.1Cre; Atg5f/f mice treated with BLM (Atg5-/- AT2-BLM) at day 14. We found the glycolytic and pentose phosphate pathways were promoted, but that the synthesis of fatty acids was repressed in mouse AT2 cells during BLM injury. Autophagy may serve as a switch between these two metabolic pathways during lung injury. These data highlight an essential role for autophagy in reprogramming the metabolism of alveolar progenitor cells to meet energy needs for alveolar epithelial regeneration. Overall design: 12 samples were analyzed. Each RNA-seq group with 3 biological replicates. Alveolar type 2 cells were sorted from Atg5f/f mice treated with PBS (AT2-PBS), Nkx2.1Cre; Atg5f/f mice treated with PBS (Atg5-/- AT2-PBS), Atg5f/f mice treated with BLM (AT2-BLM), and Nkx2.1Cre; Atg5f/f mice treated with BLM (Atg5-/- AT2-BLM) by FACS.