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10.1152/ajplung.00484.2016 http://scihub22266oqcxt.onion/10.1152/ajplung.00484.2016 C5451590!5451590 !28188225     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28188225 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inflammation-induced caveolin-1 and BMPRII depletion promotes endothelial dysfunction and TGF-?-driven pulmonary vascular remodeling |pdf=|usr=}}{{28188225 }} gab.com Text Inflammation-induced caveolin-1 and BMPRII depletion promotes endothelial dysfunction and TGF- -driven pulmonary vascular remodeling JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=28188225 #FOAvip Endothelial cell (EC) activation and vascular injury are hallmark features of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Caveolin-1 (Cav-1) is highly expressed in pulmonary microvascular ECs and plays a key role in maintaining vascular homeostasis. The aim of this study was to determine if the lung inflammatory response to Escherichia coli lipopolysaccharide (LPS) promotes priming of ECs via Cav-1 depletion and if this contributes to the onset of pulmonary vascular remodeling. To test the hypothesis that depletion of Cav-1 primes ECs to respond to profibrotic signals, C57BL6 wild-type (WT) mice (Tie2.Cre(-);Cav1(fl/fl) ) were exposed to nebulized LPS (10 mg; 1 h daily for 4 days) and compared with EC-specific Cav1(-/-) (Tie2.Cre(+);Cav1(fl/fl) ). After 96 h of LPS exposure, total lung Cav-1 and bone morphogenetic protein receptor type II (BMPRII) expression were reduced in WT mice. Moreover, plasma albumin leakage, infiltration of immune cells, and levels of IL-6/IL-6R and transforming growth factor-? (TGF-?) were elevated in both LPS-treated WT and EC-Cav1(-/-) mice. Finally, EC-Cav1(-/-) mice exhibited a modest increase in microvascular thickness basally and even more so on exposure to LPS (96 h). EC-Cav1(-/-) mice and LPS-treated WT mice exhibited reduced BMPRII expression and endothelial nitric oxide synthase uncoupling, which along with increased TGF-? promoted TGF?RI-dependent SMAD-2/3 phosphorylation. Finally, human lung sections from patients with ARDS displayed reduced EC Cav-1 expression, elevated TGF-? levels, and severe pulmonary vascular remodeling. Thus EC Cav-1 depletion, oxidative stress-mediated reduction in BMPRII expression, and enhanced TGF-?-driven SMAD-2/3 signaling promote pulmonary vascular remodeling in inflamed lungs. Twit Text FOAVip Inflammation-induced caveolin-1 and BMPRII depletion promotes endothelial dysfunction and TGF- -driven pulmonary vascular remodeling ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=28188225 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28188225 #FOAvip English Wikipedia <ref>{{Cite pmid|28188225 }}</ref> Inflammation-induced caveolin-1 and BMPRII depletion promotes endothelial dysfunction and TGF-?-driven pulmonary vascular remodeling #MMPMID28188225 Oliveira SDS ; Castellon M ; Chen J ; Bonini MG ; Gu X ; Elliott MH ; Machado RF ; Minshall RD Am J Physiol Lung Cell Mol Physiol 2017[May]; 312 (5 ): L760-L771 PMID28188225 show ga Endothelial cell (EC) activation and vascular injury are hallmark features of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Caveolin-1 (Cav-1) is highly expressed in pulmonary microvascular ECs and plays a key role in maintaining vascular homeostasis. The aim of this study was to determine if the lung inflammatory response to Escherichia coli lipopolysaccharide (LPS) promotes priming of ECs via Cav-1 depletion and if this contributes to the onset of pulmonary vascular remodeling. To test the hypothesis that depletion of Cav-1 primes ECs to respond to profibrotic signals, C57BL6 wild-type (WT) mice (Tie2.Cre(-);Cav1(fl/fl) ) were exposed to nebulized LPS (10 mg; 1 h daily for 4 days) and compared with EC-specific Cav1(-/-) (Tie2.Cre(+);Cav1(fl/fl) ). After 96 h of LPS exposure, total lung Cav-1 and bone morphogenetic protein receptor type II (BMPRII) expression were reduced in WT mice. Moreover, plasma albumin leakage, infiltration of immune cells, and levels of IL-6/IL-6R and transforming growth factor-? (TGF-?) were elevated in both LPS-treated WT and EC-Cav1(-/-) mice. Finally, EC-Cav1(-/-) mice exhibited a modest increase in microvascular thickness basally and even more so on exposure to LPS (96 h). EC-Cav1(-/-) mice and LPS-treated WT mice exhibited reduced BMPRII expression and endothelial nitric oxide synthase uncoupling, which along with increased TGF-? promoted TGF?RI-dependent SMAD-2/3 phosphorylation. Finally, human lung sections from patients with ARDS displayed reduced EC Cav-1 expression, elevated TGF-? levels, and severe pulmonary vascular remodeling. Thus EC Cav-1 depletion, oxidative stress-mediated reduction in BMPRII expression, and enhanced TGF-?-driven SMAD-2/3 signaling promote pulmonary vascular remodeling in inflamed lungs. |*Vascular Remodeling/drug effects [MESH] |Actins/metabolism [MESH] |Acute Lung Injury/complications/immunology/pathology [MESH] |Adult [MESH] |Aged [MESH] |Animals [MESH] |Bone Morphogenetic Protein Receptors, Type II/*metabolism [MESH] |Bronchoalveolar Lavage Fluid [MESH] |Caveolin 1/*metabolism [MESH] |Cell Shape/drug effects [MESH] |Cytokines/metabolism [MESH] |Endothelial Cells/drug effects/metabolism/*pathology [MESH] |Female [MESH] |Humans [MESH] |Inflammation Mediators/metabolism [MESH] |Inflammation/metabolism/*pathology [MESH] |Interleukin-6/pharmacology [MESH] |Lipopolysaccharides [MESH] |Lung/*blood supply/immunology/*metabolism/pathology [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Middle Aged [MESH] |Models, Biological [MESH] |Nitric Oxide Synthase Type III/metabolism [MESH] |Proteolysis/drug effects [MESH] |Pulmonary Artery/pathology [MESH] |Receptors, Transforming Growth Factor beta/metabolism [MESH] |Respiratory Distress Syndrome/complications/immunology/pathology [MESH] |Time Factors [MESH]Inflammation-induced caveolin-1 and BMPRII depletion promotes endothel(epmc).pdf DeepDyve Pubget Overpricing