Inhibition of autophagy enhanced cobalt chloride‑induced apoptosis in rat alveolar type II epithelial cells.

Hypoxia is a type of cellular stress that may result in apoptosis and autophagy. The molecular mechanisms underlying the association between autophagy and apoptosis remain unclear, particularly in hypoxic conditions. Transmission electron microscope, AO‑PI staining, flow cytometry and western blot were used to examine the crosstalk between autophagy and apoptosis in hypoxic conditions. Rat alveolar type II epithelial RLE‑6TN cells were cultured in a long‑term hypoxic environment established by cobalt (II) chloride. It was demonstrated that autophagy and apoptosis occurred in RLE‑6TN cells under hypoxic conditions. Treatment of RLE‑6TN cells with the autophagy inhibitor 3‑methyladenine increased the generation of reactive oxygen species, mitochondrial damage and hypoxia‑induced apoptosis. The expression of caspases, particularly caspase‑9, increased and may have participated in these processes. The data indicated that the inhibition of autophagy enhanced apoptosis through the mitochondria‑mediated intrinsic pathway. These findings provide important insight into the molecular mechanism of autophagy and apoptosis crosstalk. This may provide new insights into pulmonary disease surveillance, diagnosis and treatment. [ABSTRACT FROM AUTHOR]