title: Perfluorocarbon inhibits lipopolysaccharide-induced macrophage inflammatory protein-2 expression and activation of ATF-2 and c-Jun in A549 pulmonary epithelial cells.
abstract: The signaling pathway that mediates the anti-inflammatory effects of perfluorocarbon (PFC) in alveolar epithelial cells treated with lipopolysaccharide (LPS) remains unclear. To evaluate the role of macrophage-inflammatory protein-2 (MIP-2), four A549 treatment groups were utilized: (1) untreated control, (2) 10 μg/mL of LPS, (3) 10 μg/mL of LPS+30% PFC and (4) 30% PFC. MIP-2 mRNA expression was determined by qPCR and ELISA. Mitogen-activated protein kinase (MAPK) activation was determined by Western blot analysis, and MIP-2 expression was determined by qPCR following treatment with MAPK inhibitors. PFC suppressed LPS-induced MIP-2 mRNA levels (P≤0.035) and MIP-2 secretion (P≤0.046). LPS induced ATF-2 and c-Jun phosphorylation, which was suppressed by PFC. Finally, inhibitors of ERK, JNK, and p38 suppressed LPS-induced MIP-2 mRNA expression. Thus, PFC inhibits LPS-induced MIP-2 expression and ATF-2 and c-Jun phosphorylation. To fully explore the therapeutic potential of PFC for acute lung injury (ALI), in vivo analyses are required to confirm these effects.
authors.affiliation: Chinese People's Liberation Army General Hospital Department of Pulmonary Medicine Beijing China.
authors.forename: Y
authors.initials: Y
authors.lastname: Hu
authors.affiliation: Chinese People's Liberation Army General Hospital Department of Pulmonary Medicine Beijing China.
authors.forename: C S
authors.initials: CS
authors.lastname: Li
authors.affiliation: Chinese People's Liberation Army General Hospital Department of Pulmonary Medicine Beijing China.
authors.forename: Y Q
authors.initials: YQ
authors.lastname: Li
authors.affiliation: Chinese People's Liberation Army General Hospital Department of Pulmonary Medicine Beijing China.
authors.forename: Y
authors.initials: Y
authors.lastname: Liang
authors.affiliation: Chinese People's Liberation Army General Hospital Department of Pulmonary Medicine Beijing China.
authors.forename: L
authors.initials: L
authors.lastname: Cao
authors.affiliation: Chinese People's Liberation Army General Hospital Department of Pulmonary Medicine Beijing China chenla301@263.net.
authors.forename: L A
authors.initials: LA
authors.lastname: Chen
mesh_terms: D000072283:A549 Cells; D051698:Activating Transcription Factor 2 / Q000378:metabolism*; D015153:Blotting, Western; D054426:Chemokine CXCL2 / Q000235:genetics* / Q000378:metabolism; D004789:Enzyme Activation / Q000187:drug effects; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism*; D005466:Fluorocarbons / Q000633:toxicity*; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008168:Lung / Q000473:pathology*; D008954:Models, Biological; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
chemical_list: D051698:Activating Transcription Factor 2; D054426:Chemokine CXCL2; D005466:Fluorocarbons; D008070:Lipopolysaccharides; D047428:Protein Kinase Inhibitors; D012333:RNA, Messenger; D048031:JNK Mitogen-Activated Protein Kinases