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Full-Text Articles in Medicine and Health Sciences
Histone Deacetylase Inhibitors Prevent Pulmonary Endothelial Hyperpermeability And Acute Lung Injury By Regulating Heat Shock Protein 90 Function, Atul D. Joshi, Nektarios Barabutis, Charalampos Birmpas, Christiana Dimitropoulou, Gagan Thangjam, Mary Cherian-Shaw, John Dennison, John D. Catravas
Histone Deacetylase Inhibitors Prevent Pulmonary Endothelial Hyperpermeability And Acute Lung Injury By Regulating Heat Shock Protein 90 Function, Atul D. Joshi, Nektarios Barabutis, Charalampos Birmpas, Christiana Dimitropoulou, Gagan Thangjam, Mary Cherian-Shaw, John Dennison, John D. Catravas
Bioelectrics Publications
Transendothelial hyperpermeability caused by numerous agonists is dependent on heat shock protein 90 (Hsp90) and leads to endothelial barrier dysfunction (EBD). Inhibition of Hsp90 protects and restores transendothelial permeability. Hyperacetylation of Hsp90, as by inhibitors of histone deacetylase (HDAC), suppresses its chaperone function and mimics the effects of Hsp90 inhibitors. In this study we assessed the role of HDAC in mediating lipopolysaccharide (LPS)-induced transendothelial hyperpermeability and acute lung injury (ALI). We demonstrate that HDAC inhibition protects against LPS-mediated EBD. Inhibition of multiple HDAC by the general inhibitors panobinostat or trichostatin provided protection against LPS-induced transendothelial hyperpermeability, acetylated and suppressed Hsp90 …
Pkc-Dependent Phosphorylation Of Enos At T495 Regulates Enos Coupling And Endothelial Barrier Function In Response To G(+) -Toxins, Feng Chen, Sanjiv Kumar, Yanfang Yu, Saurabh Aggarwal, Christine Gross, Yusi Wang, Trinad Chakraborty, Alexander D. Verin, John D. Catravas, Rudolf Lucas, Stephen M. Black, David J. R. Fulton
Pkc-Dependent Phosphorylation Of Enos At T495 Regulates Enos Coupling And Endothelial Barrier Function In Response To G(+) -Toxins, Feng Chen, Sanjiv Kumar, Yanfang Yu, Saurabh Aggarwal, Christine Gross, Yusi Wang, Trinad Chakraborty, Alexander D. Verin, John D. Catravas, Rudolf Lucas, Stephen M. Black, David J. R. Fulton
Bioelectrics Publications
Gram positive (G(+)) infections make up similar to 50% of all acute lung injury cases which are characterized by extensive permeability edema secondary to disruption of endothelial cell (EC) barrier integrity. A primary cause of increased permeability are cholesterol-dependent cytolysins (CDCs) of G(+)-bacteria, such as pneumolysin (PLY) and listeriolysin-O (LLO) which create plasma membrane pores, promoting Ca2+-influx and activation of PKC alpha. In human lung microvascular endothelial cells (HLMVEC), pretreatment with the nitric oxide synthase (NOS) inhibitor, ETU reduced the ability of LLO to increase microvascular cell permeability suggesting an endothelial nitric oxide synthase (eNOS)-dependent mechanism. LLO stimulated superoxide production …
Dimethylarginine Dimethylaminohydrolase Ii Overexpression Attenuates Lps-Mediated Lung Leak In Acute Lung Injury, Saurabh Aggarwal, Christine M. Gross, Sanjiv Kumar, Christiana Dimitropoulou, Shruti Sharma, Boris A. Gorshkov, Supriya Sridhar, Qing Lu, Natalia V. Bogatcheva, Agnieszka J. Jezierska-Drutel, Rudolf Lucas, John D. Catravas, Stephen M. Black
Dimethylarginine Dimethylaminohydrolase Ii Overexpression Attenuates Lps-Mediated Lung Leak In Acute Lung Injury, Saurabh Aggarwal, Christine M. Gross, Sanjiv Kumar, Christiana Dimitropoulou, Shruti Sharma, Boris A. Gorshkov, Supriya Sridhar, Qing Lu, Natalia V. Bogatcheva, Agnieszka J. Jezierska-Drutel, Rudolf Lucas, John D. Catravas, Stephen M. Black
Bioelectrics Publications
Acute lung injury (ALI) is a severe hypoxemic respiratory insufficiency associated with lung leak, diffuse alveolar damage, inflammation, and loss of lung function. Decreased dimethylaminohydrolase (DDAH) activity and increases in asymmetric dimethylarginine (ADMA), together with exaggerated oxidative/nitrative stress, contributes to the development of ALI in mice exposed to LPS. Whether restoring DDAH function and suppressing ADMA levels can effectively ameliorate vascular hyperpermeability and lung injury in ALI is unknown, and was the focus of this study. In human lung microvascular endothelial cells, DDAH II overexpression prevented the LPS-dependent increase in ADMA, superoxide, peroxynitrite, and protein nitration. DDAH II also attenuated …