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dc.contributor.authorYang, Guang
dc.contributor.authorHamacher, Jürg
dc.contributor.authorGorshkov, Boris A
dc.contributor.authorWhite, Richard E.
dc.contributor.authorSridhar, Supriya
dc.contributor.authorVerin, Alexander D.
dc.contributor.authorChakraborty, Trinad
dc.contributor.authorLucas, Rudolf
dc.date.accessioned2012-10-26T16:26:54Z
dc.date.available2012-10-26T16:26:54Z
dc.date.issued2010en_US
dc.identifier.citationJ Cardiovasc Dis Res. 2010 Jan-Mar; 1(1):29-36en_US
dc.identifier.issn0976-2833en_US
dc.identifier.pmid21188088en_US
dc.identifier.doi10.4103/0975-3583.59983en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/617
dc.description.abstractAbstract: Pulmonary edema, a major manifestation of left ventricular heart failure, renal insufficiency, shock, diffuse alveolar damage and lung hypersensitivity states, is a significant medical problem worldwide and can be life-threatening. The proinflammatory cytokine tumor necrosis factor (TNF) has been shown to contribute to the pathogenesis and development of pulmonary edema. However, some recent studies have demonstrated surprisingly that TNF can also promote alveolar fluid reabsorption in vivo and in vitro. This protective effect of the cytokine is mediated by the lectin-like domain of the cytokine, which is spatially distinct from the TNF receptor binding sites. The TIP peptide, a synthetic mimic of the lectin-like domain of TNF, can significantly increase alveolar fluid clearance and improve lung compliance in pulmonary edema models. In this review, we will discuss the dual role of TNF in pulmonary edema.
dc.description.abstractAbbreviations: - tumor necrosis factor (TNF); acute lung injury (ALI); acute respiratory distress syndrome (ARDS); positive end-expiratory pressure (PEEP);epithelial sodium channel (ENaC);neural precursor cell-expressed developmentally downregulated (gene 4) protein (Nedd4-2);serum and glucocorticoid dependent kinase (Sgk-1);insulin-like growth factor 1 (IGF-1);Protein Kinase C (PKC);reactive oxygen species (ROS);myosin light chain (MLC);pneumolysin (PLY);listeriolysin (LLO);interleukin (IL);bronchoalveolar lavage fluids (BALF);Bacillus Calmette-Guerin (BCG);TNF receptor type 1 (TNFR1); TNF receptor type 2 (TNF-R2);
dc.rights© Journal of Cardiovascular Disease Researchen_US
dc.subjectInvited Reviewen_US
dc.titleThe Dual Role of TNF in Pulmonary Edemaen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3004168en_US
dc.contributor.corporatenameDepartment of Pharmacology and Toxicology
dc.contributor.corporatenameVascular Biology Center
refterms.dateFOA2019-04-10T07:49:43Z
html.description.abstractAbstract: Pulmonary edema, a major manifestation of left ventricular heart failure, renal insufficiency, shock, diffuse alveolar damage and lung hypersensitivity states, is a significant medical problem worldwide and can be life-threatening. The proinflammatory cytokine tumor necrosis factor (TNF) has been shown to contribute to the pathogenesis and development of pulmonary edema. However, some recent studies have demonstrated surprisingly that TNF can also promote alveolar fluid reabsorption in vivo and in vitro. This protective effect of the cytokine is mediated by the lectin-like domain of the cytokine, which is spatially distinct from the TNF receptor binding sites. The TIP peptide, a synthetic mimic of the lectin-like domain of TNF, can significantly increase alveolar fluid clearance and improve lung compliance in pulmonary edema models. In this review, we will discuss the dual role of TNF in pulmonary edema.
html.description.abstractAbbreviations: - tumor necrosis factor (TNF); acute lung injury (ALI); acute respiratory distress syndrome (ARDS); positive end-expiratory pressure (PEEP);epithelial sodium channel (ENaC);neural precursor cell-expressed developmentally downregulated (gene 4) protein (Nedd4-2);serum and glucocorticoid dependent kinase (Sgk-1);insulin-like growth factor 1 (IGF-1);Protein Kinase C (PKC);reactive oxygen species (ROS);myosin light chain (MLC);pneumolysin (PLY);listeriolysin (LLO);interleukin (IL);bronchoalveolar lavage fluids (BALF);Bacillus Calmette-Guerin (BCG);TNF receptor type 1 (TNFR1); TNF receptor type 2 (TNF-R2);


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