{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kovacs-Kasa A"],"funding":["American Heart Association","American Heart Association-American Stroke Association","NHLBI NIH HHS","NIH HHS"],"pagination":["2893-2905"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9946131"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["236(4)"],"pubmed_abstract":["Acute lung injury (ALI) is an acute inflammatory process arises from a wide range of lung insults. A major cause of ALI is dysfunction of the pulmonary vascular endothelial barrier but the mechanisms involved are incompletely understood. The therapeutic potential of histone deacetylase (HDAC) inhibitors for the treatment of cardiovascular and inflammatory diseases is increasingly apparent, but the mechanisms by which HDACs regulate pulmonary vascular barrier function remain to be resolved. We found that specific Class IIa HDACs inhibitor, TMP269, significantly attenuated the lipopolysaccharide (LPS)-induced human lung microvascular endothelial cells (HLMVEC) barrier compromise in vitro and improved vascular barrier integrity and lung function in murine model of ALI in vivo. TMP269 decrease"],"journal":["Journal of cellular physiology"],"pubmed_title":["Inhibition of Class IIa HDACs improves endothelial barrier function in endotoxin-induced acute lung injury."],"pmcid":["PMC9946131"],"funding_grant_id":["P01 HL101902","18CDA34110225","18POST33990193","R01 HL134934","NIH: HL101902"],"pubmed_authors":["Fulton DJ","Cherian-Shaw M","Kovacs-Kasa A","Kovacs L","Verin AD","Patel V","Meadows ML","Su Y"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of Class IIa HDACs improves endothelial barrier function in endotoxin-induced acute lung injury.","description":"Acute lung injury (ALI) is an acute inflammatory process arises from a wide range of lung insults. A major cause of ALI is dysfunction of the pulmonary vascular endothelial barrier but the mechanisms involved are incompletely understood. The therapeutic potential of histone deacetylase (HDAC) inhibitors for the treatment of cardiovascular and inflammatory diseases is increasingly apparent, but the mechanisms by which HDACs regulate pulmonary vascular barrier function remain to be resolved. We found that specific Class IIa HDACs inhibitor, TMP269, significantly attenuated the lipopolysaccharide (LPS)-induced human lung microvascular endothelial cells (HLMVEC) barrier compromise in vitro and improved vascular barrier integrity and lung function in murine model of ALI in vivo. TMP269 decrease","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2025-04-04T00:02:49.775Z","creation":"2025-04-04T00:02:49.775Z"},"accession":"S-EPMC9946131","cross_references":{"pubmed":["32959895"],"doi":["10.1002/jcp.30053"]}}