{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mumby S"],"funding":["Royal Brompton Hospital Charitable Fund","British Heart Foundation","Wellcome Trust Programme","European Respiratory Society Long-Term Fellowship","Imperial College London","National Funding Agency for Research","Wellcome Trust","NIHR Respiratory Disease Biomedical Research Unit at the Royal Brompton","Harefield NHS Foundation Trust"],"pagination":["157-164"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5215513"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22(1)"],"pubmed_abstract":["Background and objective
Nuclear factor kappa B (NF-kB)-mediated inflammatory gene expression and vascular endothelial cell proliferation/remodelling are implicated in the pathophysiology of the fatal disease, pulmonary arterial hypertension (PAH). Bromodomain and extra-terminal (BET) proteins are essential for the expression of a subset of NF-kB-induced inflammatory genes. BET mimics including JQ1+ prevent binding of BETs to acetylated histones and down-regulate the expression of selected genes.Methods
The effects of JQ1+ on the proliferation of primary human pulmonary microvascular endothelial cells (HPMECs) from healthy subjects were measured by bromodeoxyuridine (BrdU) incorporation. Cell cycle progression was assessed by flow cytometry; mRNA and protein levels of cycli"],"journal":["Respirology (Carlton, Vic.)"],"pubmed_title":["Bromodomain and extra-terminal protein mimic JQ1 decreases inflammation in human vascular endothelial cells: Implications for pulmonary arterial hypertension."],"pmcid":["PMC5215513"],"funding_grant_id":["093080/Z/10/","093080/Z/10/Z","PG/14/27/30679","ANR-JSV1-001"],"pubmed_authors":["Adcock IM","Meng C","Gambaryan N","Perros F","Mumby S","Humbert M","Wort SJ"],"additional_accession":[]},"is_claimable":false,"name":"Bromodomain and extra-terminal protein mimic JQ1 decreases inflammation in human vascular endothelial cells: Implications for pulmonary arterial hypertension.","description":"Background and objective
Nuclear factor kappa B (NF-kB)-mediated inflammatory gene expression and vascular endothelial cell proliferation/remodelling are implicated in the pathophysiology of the fatal disease, pulmonary arterial hypertension (PAH). Bromodomain and extra-terminal (BET) proteins are essential for the expression of a subset of NF-kB-induced inflammatory genes. BET mimics including JQ1+ prevent binding of BETs to acetylated histones and down-regulate the expression of selected genes.Methods
The effects of JQ1+ on the proliferation of primary human pulmonary microvascular endothelial cells (HPMECs) from healthy subjects were measured by bromodeoxyuridine (BrdU) incorporation. Cell cycle progression was assessed by flow cytometry; mRNA and protein levels of cycli","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Jan","modification":"2025-04-05T14:13:17.951Z","creation":"2019-03-27T02:33:16Z"},"accession":"S-EPMC5215513","cross_references":{"pubmed":["27539364"],"doi":["10.1111/resp.12872"]}}