Background: Pulmonary arterial hypertension (PAH) is characterised by pulmonary vascular remodelling and inflammation. Bromodomain and extra-terminal (BET) proteins regulate a subset of NF-kB-induced inflammatory genes. JQ1, a BET mimic, prevents BET binding to acetylated histones to down-regulate selected genes. Methods: Immunohistochemical staining of human lung (N=14 PAH and N=12 non-PAH) was performed for BRD2/4. Cultured human pulmonary microvascular endothelial cells (HPMEC) and artery smooth muscle cells (HPASMC) from PAH patients (N=4) and non-PAH controls (N=4) were stimulated with TNF? ± JQ1. IL-6 and -8 mRNA/protein was measured by RT-qPCR/ELISA. Chromatin immunoprecipitation was also performed. Results: Nuclear BRD2 and BRD4 levels were significantly (p<0.0001) increased in the endothelium and smooth muscle cells of PAH patients compared to controls. TNF?-driven IL-6 release from both HPMECs and HPASMCs was greater in PAH cells than control cells with greater IL-6 mRNA levels being induced in cells from control subjects, whereas the opposite was true for CXCL8/IL-8. TNF?-induced NF-?B activation and recruitment of activated NF-?B p65 to the IL-6 and CXCL8/IL-8 promoters was similar in both cell types and between subject groups. JQ1 suppressed TNF?-induced IL-6 and IL-8 release and mRNA expression to a comparable extent in control and PAH HPMECs and HPASMCs. In HPMECs the IC50 for JQ1 suppression of IL-8 release was 3-times higher (~300nM) than that for IL-6 (~100nM) whereas the IC50 for IL-6 suppression in HPASMCs was double that for IL-8 suppression (~200 vs ~100nM). Conclusion: BET proteins could be a future target for PAH.