ArticleThe American journal of pathology2002
Activator protein-1 activation in acute lung injury.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
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- Glucocorticoid Treatment in Acute Respiratory Distress Syndrome: An Overview on Mechanistic Insights and Clinical Benefit.International journal of molecular sciences · 2023Review
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- Single-cell RNA sequencing identifies macrophage transcriptional heterogeneities in granulomatous diseases.The European respiratory journal · 2021Article
- Cigarette Smoke and Nicotine-Containing Electronic-Cigarette Vapor Downregulate Lung WWOX Expression, Which Is Associated with Increased Severity of Murine Acute Respiratory Distress Syndrome.American journal of respiratory cell and molecular biology · 2021Article
- The Crucial Role of PPARγ-Egr-1-Pro-Inflammatory Mediators Axis in IgG Immune Complex-Induced Acute Lung Injury.Frontiers in immunology · 2021Article
- Chinese Herbs and Repurposing Old Drugs as Therapeutic Agents in the Regulation of Oxidative Stress and Inflammation in Pulmonary Diseases.Journal of inflammation research · 2021Review
- Transcription factor-mediated signaling pathways' contribution to the pathology of acute lung injury and acute respiratory distress syndrome.American journal of translational research · 2020Article
- Loss of lung WWOX expression causes neutrophilic inflammation.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Continuous blood purification treatment for endotoxin-induced acute respiratory distress syndrome.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017Article
- Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 Regulates LPS-Induced Inflammation and Alveolar Remodeling in the Developing Lung.American journal of respiratory cell and molecular biology · 2016Article
- Apigenin inhibits PMA-induced expression of pro-inflammatory cytokines and AP-1 factors in A549 cells.Molecular and cellular biochemistry · 2015Article
- Inhibition of neutrophil exocytosis ameliorates acute lung injury in rats.Shock (Augusta, Ga.) · 2013Article
- CCAAT/enhancer-binding protein δ is a critical mediator of lipopolysaccharide-induced acute lung injury.The American journal of pathology · 2013Article
- Critical role for CCAAT/enhancer-binding protein β in immune complex-induced acute lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- An essential role for Stat3 in regulating IgG immune complex-induced pulmonary inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Molecular mechanisms of inflammation and tissue injury after major trauma--is complement the "bad guy"?Journal of biomedical science · 2011Review
- Surfactant blocks lipopolysaccharide signaling by inhibiting both NFκB and PARP activation in experimental ARDS.Molecular and cellular biochemistry · 2011Article
- Activation of the transcription factor FosB/activating protein-1 (AP-1) is a prominent downstream signal of the extracellular nucleotide receptor P2RX7 in monocytic and osteoblastic cells.The Journal of biological chemistry · 2010Article
- Cell signaling via the P2X(7) nucleotide receptor: linkage to ROS production, gene transcription, and receptor trafficking.Purinergic signalling · 2009Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The role of activator protein-1 (AP-1) in inflammation is primarily unknown. AP-1 was evaluated in nuclear extracts from alveolar macrophages and whole lung nuclear extracts during acute lung injury after deposition of IgG immune complexes. AP-1 activation occurred in macrophages and in whole lung extracts, but with distinctly different time courses. Low levels of constitutive AP-1 were observed in normal rat lung as determined by the electrophoretic mobility shift assay. Increased AP-1 was detected 2 hours after initiation of the inflammatory response in lung with a further increase by 4 hours, while AP-1 activation was found in alveolar macrophages 0.5 hour after onset of the inflammatory response. mRNAs and proteins for c-fos, c-jun, jun-B, and jun-D were all up-regulated in whole lung tissues and in alveolar macrophages during acute lung injury induced by IgG immune complex deposition. Depletion of lung macrophages sharply reduced AP-1 activation, as did anti-tumor necrosis factor-alpha, whereas complement depletion showed no effect on lung AP-1 activation. The data suggest that activation of AP-1 occurs in both alveolar macrophages and in the lung, and this activation process is macrophage- and tumor necrosis factor-alpha-dependent.
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Registered trials
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