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10.1165/rcmb.2016-0236RC http://scihub22266oqcxt.onion/10.1165/rcmb.2016-0236RC C5105187!5105187 !27556883     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27556883 &cmd=llinks): Failed to open stream: HTTP request failed! 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An Inhaled Inhibitor of Myristoylated Alanine-Rich C Kinase Substrate Reverses LPS-Induced Acute Lung Injury in Mice |pdf=|usr=}}{{27556883 }} gab.com Text An Inhaled Inhibitor of Myristoylated Alanine-Rich C Kinase Substrate Reverses LPS-Induced Acute Lung Injury in Mice JO: Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=27556883 #FOAvip Intratracheal instillation of bacterial LPS is a well-established model of acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS). Because the myristoylated alanine-rich C kinase substrate (MARCKS) protein is involved in neutrophil migration and proinflammatory cytokine production, we examined whether an aerosolized peptide that inhibits MARCKS function could attenuate LPS-induced lung injury in mice. The peptide, BIO-11006, was delivered at 50 ?M via inhalation either just before intratracheal instillation of 5 ?g of LPS into Balb/C mice, or 4, 12, 24, or 36 hours after LPS instillation. Effects of BIO-11006 were evaluated via analysis of mouse disease-related behavior, lung histology, bronchoalveolar lavage fluid total protein, neutrophil counts and percentages, cytokine (KC [CXCl1, mouse IL-8 equivalent] and TNF-?) expression, and activation of NF-?B in lung tissue. Treatment with aerosolized BIO-11006 at 0, 4, 12, 24, and even 36 hours after LPS instillation reversed the disease process: mouse behavior returned to normal after two treatments 12 hours apart with the inhaled peptide after LPS injury, whereas control LPS-instilled animals treated with PBS only remained moribund. Histological appearance of inflammation, bronchoalveolar lavage fluid protein levels, leukocyte and neutrophil numbers, KC and TNF-? gene and protein expression, and NF-?B activation were all significantly attenuated by inhaled BIO-11006 at all time points. These results implicate MARCKS protein in the pathogenesis of ALI/ARDS and suggest that MARCKS-inhibitory peptide(s), delivered by inhalation, could represent a new and potent therapeutic treatment for ALI/ARDS, even if administered well after the disease process has begun. Twit Text FOAVip An Inhaled Inhibitor of Myristoylated Alanine-Rich C Kinase Substrate Reverses LPS-Induced Acute Lung Injury in Mice ????Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=27556883 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27556883 #FOAvip English Wikipedia <ref>{{Cite pmid|27556883 }}</ref> An Inhaled Inhibitor of Myristoylated Alanine-Rich C Kinase Substrate Reverses LPS-Induced Acute Lung Injury in Mice #MMPMID27556883 Yin Q ; Fang S ; Park J ; Crews AL ; Parikh I ; Adler KB Am J Respir Cell Mol Biol 2016[Nov]; 55 (5 ): 617-622 PMID27556883 show ga Intratracheal instillation of bacterial LPS is a well-established model of acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS). Because the myristoylated alanine-rich C kinase substrate (MARCKS) protein is involved in neutrophil migration and proinflammatory cytokine production, we examined whether an aerosolized peptide that inhibits MARCKS function could attenuate LPS-induced lung injury in mice. The peptide, BIO-11006, was delivered at 50 ?M via inhalation either just before intratracheal instillation of 5 ?g of LPS into Balb/C mice, or 4, 12, 24, or 36 hours after LPS instillation. Effects of BIO-11006 were evaluated via analysis of mouse disease-related behavior, lung histology, bronchoalveolar lavage fluid total protein, neutrophil counts and percentages, cytokine (KC [CXCl1, mouse IL-8 equivalent] and TNF-?) expression, and activation of NF-?B in lung tissue. Treatment with aerosolized BIO-11006 at 0, 4, 12, 24, and even 36 hours after LPS instillation reversed the disease process: mouse behavior returned to normal after two treatments 12 hours apart with the inhaled peptide after LPS injury, whereas control LPS-instilled animals treated with PBS only remained moribund. Histological appearance of inflammation, bronchoalveolar lavage fluid protein levels, leukocyte and neutrophil numbers, KC and TNF-? gene and protein expression, and NF-?B activation were all significantly attenuated by inhaled BIO-11006 at all time points. These results implicate MARCKS protein in the pathogenesis of ALI/ARDS and suggest that MARCKS-inhibitory peptide(s), delivered by inhalation, could represent a new and potent therapeutic treatment for ALI/ARDS, even if administered well after the disease process has begun. |Acute Lung Injury/*chemically induced/*drug therapy [MESH] |Aerosols/administration & dosage/pharmacology [MESH] |Animals [MESH] |Behavior, Animal [MESH] |Bronchoalveolar Lavage Fluid [MESH] |Cytokines/metabolism [MESH] |Female [MESH] |Inflammation Mediators/metabolism [MESH] |Intracellular Signaling Peptides and Proteins/*antagonists & inhibitors/metabolism [MESH] |Leukocytes/metabolism [MESH] |Lipopolysaccharides [MESH] |Lung/drug effects/metabolism/pathology [MESH] |Membrane Proteins/*antagonists & inhibitors/metabolism [MESH] |Mice, Inbred BALB C [MESH] |Myristoylated Alanine-Rich C Kinase Substrate [MESH] |NF-kappa B/metabolism [MESH]An Inhaled Inhibitor of Myristoylated Alanine-Rich C Kinase Substrate (epmc).pdf DeepDyve Pubget Overpricing