biostudies-literatureMumby SRoyal Brompton Hospital Charitable FundBritish Heart FoundationWellcome Trust ProgrammeEuropean Respiratory Society Long-Term FellowshipImperial College LondonNational Funding Agency for ResearchWellcome TrustNIHR Respiratory Disease Biomedical Research Unit at the Royal BromptonHarefield NHS Foundation Trust157-164https://www.ebi.ac.uk/biostudies/studies/S-EPMC5215513biostudies-literatureUnknown22(1)<h4>Background and objective</h4>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.<h4>Methods</h4>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 cycliRespirology (Carlton, Vic.)Bromodomain and extra-terminal protein mimic JQ1 decreases inflammation in human vascular endothelial cells: Implications for pulmonary arterial hypertension.PMC5215513093080/Z/10/093080/Z/10/ZPG/14/27/30679ANR-JSV1-001Adcock IMMeng CGambaryan NPerros FMumby SHumbert MWort SJfalseBromodomain and extra-terminal protein mimic JQ1 decreases inflammation in human vascular endothelial cells: Implications for pulmonary arterial hypertension.<h4>Background and objective</h4>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.<h4>Methods</h4>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 cycli2017-01-01T00:00:00Z2017 Jan2025-04-05T14:13:17.951Z2019-03-27T02:33:16ZS-EPMC52155132753936410.1111/resp.12872