TY - JOUR T1 - Placenta growth factor promotes autophagy in lung epithelial cell through JNK and p38 MAPK pathway JF - European Respiratory Journal JO - Eur Respir J VL - 42 IS - Suppl 57 SP - P3892 AU - Shih-Lung Cheng Y1 - 2013/09/01 UR - http://erj.ersjournals.com/content/42/Suppl_57/P3892.abstract N2 - Purpose: Increased placenta growth factor (PlGF) level was discovered in patients with chronic obstructive pulmonary disease (COPD). Autophagy was emerging importance in pulmonary disease, exp COPD. However, underlying mechanism between PlGF and autophagy was still unknown.Materials and Methods: In this study, the stimulated concentrations of PlGF were 25, 50, 100 pg/ml respectively for apoptosis detection in human lung epithelial cells (S-cells). Quantification with autophagy was measured by the Fluorescein microscope for GFP detection and LC3B II expression. Besides, signaling pathways with different kinases were also assayed with ELISA and Western Blotting. Besides, in vivo with animal study with instillation procine pancreatic elastase (PPE) from trachea was also performed for evaluation.Results: In cultured human bronchial epithelial cells, PlGF (dose: 100ng/ml) induced LC3B II expression by over 3-fold (p<0.01) at 12 hours stimulation. The increased JNK and p38 MAPK expression upon PlGF treatment was significantly increased with time-dependent manner (12 to 24 hour) and LC3B II expression was inhibited by the blocker agents with JNK and p38 MAPK. Besides, in vivo study, autophagosomes increased formation in mice tissues after PPE treatment and reduced after JNK and p38 MAPK blockers.Conclusion: Our findings revealed that PlGF induced autophagy with LC3B II over-expression in vitro and vivo study and underlying mechanism was via JNK and p38 MAPK signaling cascades. Further studies should be performed in human lung tissue for confirmation. ER -