Research Paper Volume 10, Issue 8 pp 2098—2112

Impaired autophagic activity and ATG4B deficiency are associated with increased endoplasmic reticulum stress-induced lung injury

Figure 5. Tunicamycin treatment induces ER stress but not autophagy in lungs from Atg4b-/- mice. (A) Representative immunoblots of ER stress biomarkers in lung tissue from WT vehicle-control and WT tunicamycin-treated mice at 3 days post-challenge. (B) Representative immunoblots of ER stress biomarkers in lung tissue from Atg4b vehicle-control and Atg4b tunicamycin-treated null mice at 3 days post-challenge. (C) Representative immunoblots of ATG4B, LC3-I/ II, and p62 in lung tissue from WT vehicle-control and WT tunicamycin-treated mice at 3 days post-challenge. (D) Representative immunoblots of ATG4B, LC3-I/ II, and p62 in lung tissue from WT compared to Atg4b null mice after 3 days of tunicamycin treatment. β-tubulin was used as loading control in all experiments. Densitometry analysis (bottom panels). Results are shown as mean ± SD. Statistical significance was determined by Student´s t-test (*p < 0.05).