ArticleRespirology (Carlton, Vic.)2017
Bromodomain and extra-terminal protein mimic JQ1 decreases inflammation in human vascular endothelial cells: Implications for pulmonary arterial hypertension.
Article in Respirology (Carlton, Vic.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 65 citations in OpenAlex.
- BET inhibitors in cardiovascular diseases: from atherosclerosis to heart failure.Pharmacological reports : PR · 2026Review
- Pulmonary Arterial Hypertension: Reconfiguring the Vascular Landscape to Reverse Remodeling.Cells · 2026Article
- NF-κB signaling as a critical inflammatory node in pulmonary arterial hypertension: from vascular remodeling to right heart failure.Frontiers in immunology · 2026Review
- NF-κB and pulmonary hypertension: Advances in mechanistic research and therapeutic applications.American heart journal plus : cardiology research and practice · 2025Review
- Precision Medicine for Pulmonary Vascular Disease: The Future Is Now (2023 Grover Conference Series).Pulmonary circulation · 2025Article
- JQ1 attenuates contrast-induced acute kidney injury through the upregulation of autophagy and inhibition of inflammation.International urology and nephrology · 2024Article
- Emerging Epigenetic Targets and Their Molecular Impact on Vascular Remodeling in Pulmonary Hypertension.Cells · 2024Review
- Altered Smooth Muscle Cell Histone Acetylome by the SPHK2/S1P Axis Promotes Pulmonary Hypertension.Circulation research · 2023Article
- BRD4 as a Therapeutic Target in Pulmonary Diseases.International journal of molecular sciences · 2023Review
- Differential responses of pulmonary vascular cells from PAH patients and controls to TNFα and the effect of the BET inhibitor JQ1.Respiratory research · 2023Article
- Transcriptomic Study on the Lungs of Broilers with Ascites Syndrome.Animals : an open access journal from MDPI · 2023Article
- Integrating epigenetics and metabolomics to advance treatments for pulmonary arterial hypertension.Biochemical pharmacology · 2022Review
- TRPM3-Induced Gene Transcription Is under Epigenetic Control.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Three-dimensional CRISPR screening reveals epigenetic interaction with anti-angiogenic therapy.Communications biology · 2021Article
- The BET family in immunity and disease.Signal transduction and targeted therapy · 2021Review
- The BRD4 inhibitor JQ1 protects against chronic obstructive pulmonary disease in mice by suppressing NF-κB activation.Histology and histopathology · 2021Article
- Epigenetic Targets for Oligonucleotide Therapies of Pulmonary Arterial Hypertension.International journal of molecular sciences · 2020Review
- The therapeutic potential of BRD4 in cardiovascular disease.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Review
- Oxidative Stress and New Pathogenetic Mechanisms in Endothelial Dysfunction: Potential Diagnostic Biomarkers and Therapeutic Targets.Journal of clinical medicine · 2020Review
- Anti-Diabetic Atherosclerosis by Inhibiting High Glucose-Induced Vascular Smooth Muscle Cell Proliferation via Pin1/BRD4 Pathway.Oxidative medicine and cellular longevity · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
objectiveNuclear 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.
methodsThe 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 cyclin-dependent kinases (CDKs), inhibitors and cytokines were determined by reverse transcription-quantitative PCR (RT-qPCR), Western blotting or ELISA. Histone acetyltransferase (HAT) and deacetylase (HDAC) activities were determined in nuclear extracts from whole lung of PAH and control patients.
resultsJQ1+ significantly inhibited IL6 and IL8 (IL6 and CXCL8) mRNA and protein in HPMECs compared with its inactive enantiomer JQ1-. JQ1+ decreased NF-kB p65 recruitment to native IL6 and IL8 promoters. JQ1+ showed a concentration-dependent decrease in HPMEC proliferation compared with JQ1--treated cells. JQ1+ induced G1 cell cycle arrest by increasing the expression of the CDK inhibitors (CDKN) 1A (p21
conclusionInhibition of BETs in primary HPMECs decreases inflammation and remodelling. BET proteins could be a target for future therapies for PAH.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.