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Full-Text Articles in Medicine and Health Sciences
Endothelial Cell-Derived Extracellular Vesicles Impair The Angiogenic Response Of Coronary Artery Endothelial Cells, Nigeste Carter, Allison H. Mathiesen, Noel Miller, Michael Brown, Ruben M.L. Colunga Biancatelli, John D. Catravas, Anca D. Dobrian
Endothelial Cell-Derived Extracellular Vesicles Impair The Angiogenic Response Of Coronary Artery Endothelial Cells, Nigeste Carter, Allison H. Mathiesen, Noel Miller, Michael Brown, Ruben M.L. Colunga Biancatelli, John D. Catravas, Anca D. Dobrian
Bioelectrics Publications
Cardiovascular disease (CVD) is the most prominent cause of death of adults in the United States with coronary artery disease being the most common type of CVD. Following a myocardial event, the coronary endothelium plays an important role in the recovery of the ischemic myocardium. Specifically, endothelial cells (EC) must be able to elicit a robust angiogenic response necessary for tissue revascularization and repair. However, local or distant cues may prevent effective revascularization. Extracellular vesicles (EV) are produced by all cells and endothelium is a rich source of EVs that have access to the main circulation thereby potentially impacting local …
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 …