ArticleBritish journal of pharmacology2010
Cigarette smoke exposure up-regulates endothelin receptor B in human pulmonary artery endothelial cells: molecular and functional consequences.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
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- Doxorubicin alters G-protein coupled receptor-mediated vasocontraction in rat coronary arteries.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Role of prostanoids, nitric oxide and endothelin pathways in pulmonary hypertension due to COPD.Frontiers in medicine · 2023Review
- IL-11 system participates in pulmonary artery remodeling and hypertension in pulmonary fibrosis.Respiratory research · 2022Article
- Chronic Obstructive Pulmonary Disease and the Cardiovascular System: Vascular Repair and Regeneration as a Therapeutic Target.Frontiers in cardiovascular medicine · 2021Review
- TIMP-1: A Circulating Biomarker for Pulmonary Hypertension Diagnosis Among Chronic Obstructive Pulmonary Disease Patients.Frontiers in medicine · 2021Article
- Smoking and the Pathophysiology of Peripheral Artery Disease.Frontiers in cardiovascular medicine · 2021Review
- MUC1 deficiency mediates corticosteroid resistance in chronic obstructive pulmonary disease.Respiratory research · 2018Article
- Effects of cigarette smoke on pulmonary endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2018Review
- Non-neuronal cholinergic system contributes to corticosteroid resistance in chronic obstructive pulmonary disease patients.Respiratory research · 2016Article
- The heart as an extravascular target of endothelin-1 in particulate matter-induced cardiac dysfunction.Pharmacology & therapeutics · 2016Review
- Roflumilast improves corticosteroid resistance COPD bronchial epithelial cells stimulated with toll like receptor 3 agonist.Respiratory research · 2015Article
- A comprehensive review: the evolution of animal models in pulmonary hypertension research; are we there yet?Pulmonary circulation · 2013Review
- An eicosanoid-centric view of atherothrombotic risk factors.Cellular and molecular life sciences : CMLS · 2012Review
- Article
- PGC-1α induction in pulmonary arterial hypertension.Oxidative medicine and cellular longevity · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposePulmonary arteries from smokers and chronic obstructive pulmonary disease patients show abnormal endothelium-dependent vascular reactivity. We studied the effect of cigarette smoke extract (CSE) on endothelin receptor B (ET(B) ) expression in human pulmonary artery endothelial cells (HPAECs) and its role in endothelial dysfunction. EXPERIMENTAL APPROACH: ET(B) receptor expression was measured by real time RT-PCR, Western blot and immunofluorescence. Cell contraction, intracellular Ca(2+) , F/G-actin, RhoA activity, myosin light chain phosphorylation, ET, NO, thromboxane (Tx)A(2) and reactive oxygen species (ROS) were measured by traction microscopy, fluorescence microscopy, phalloidin fluorescence, colorimetric assay, Western blot, elisa and DCFDA fluorescence respectively. KEY
resultsCigarette smoke extract dose-dependently increased ET(B) receptor expression in HPAECs after 24h incubation. CSE-induced ET(B) expression was attenuated by bosentan, the ET(B) receptor antagonist BQ788, the Rho kinase antagonist Y27632 and the antioxidant N-acetylcysteine. A monoclonal antibody to ET-1 prevented CSE-induced ET(B) receptor overexpression. Twenty-four hour exposure to ET-1 dose-dependently increased ET(B) receptor expression, mimicking the effect of CSE. CSE-induced ET(B) receptor overexpression caused greater cell contraction; increased intracellular Ca(2+) ; increased F/G-actin and RhoA activity; increased myosin light chain phosphorylation; augmented TxA(2) and ROS production; and decreased NO after acute ET-1 (10nM). These effects were attenuated by bosentan, BQ788, Y27632 and N-acetylcysteine. CONCLUSIONS AND IMPLICATION: Cigarette smoke extract induced ET(B) receptor overexpression by a feed forward mechanism mediated partly by ET release, promoting HPAEC dysfunction and attenuated by ET(B) receptor blockade, Rho kinase and ROS inhibition. These results provide support for the use of bosentan in CS-related endothelial dysfunction.
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