ArticleCirculation2005
Development of occlusive neointimal lesions in distal pulmonary arteries of endothelin B receptor-deficient rats: a new model of severe pulmonary arterial hypertension.
Article in Circulation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 65 citations in OpenAlex.
- The emerging role of NOTCH3 receptor signalling in human lung diseases.Expert reviews in molecular medicine · 2022Review
- Characteristics of Pulmonary Vascular Remodeling in a Novel Model of Shunt-Associated Pulmonary Arterial Hypertension.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- A current view of G protein-coupled receptor - mediated signaling in pulmonary hypertension: finding opportunities for therapeutic intervention.Vessel plus · 2018Article
- Challenges in the development of chronic pulmonary hypertension models in large animals.Pulmonary circulation · 2017Article
- Molecular pathogenesis and current pathology of pulmonary hypertension.Heart failure reviews · 2016Review
- Erythropoietin upregulation in pulmonary arterial hypertension.Pulmonary circulation · 2014Article
- Arterial wall stress controls NFAT5 activity in vascular smooth muscle cells.Journal of the American Heart Association · 2014Article
- Article
- Vascular histomolecular analysis by sequential endoarterial biopsy in a shunt model of pulmonary hypertension.Pulmonary circulation · 2013Article
- Vascular endothelin receptor type B: structure, function and dysregulation in vascular disease.Biochemical pharmacology · 2012Review
- Improved pulmonary vascular reactivity and decreased hypertrophic remodeling during nonhypercapnic acidosis in experimental pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Indispensable roles of OX40L-derived signal and epistatic genetic effect in immune-mediated pathogenesis of spontaneous pulmonary hypertension.BMC immunology · 2011Article
- Emergence of fibroblasts with a proinflammatory epigenetically altered phenotype in severe hypoxic pulmonary hypertension.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Therapeutic efficacy of TBC3711 in monocrotaline-induced pulmonary hypertension.Respiratory research · 2011Article
- Hemodynamic and histologic characterization of a swine (Sus scrofa domestica) model of chronic pulmonary arterial hypertension.Comparative medicine · 2011Article
- Estrogens and development of pulmonary hypertension: interaction of estradiol metabolism and pulmonary vascular disease.Journal of cardiovascular pharmacology · 2010Review
- The xanthine derivative KMUP-1 inhibits models of pulmonary artery hypertension via increased NO and cGMP-dependent inhibition of RhoA/Rho kinase.British journal of pharmacology · 2010Article
- Interleukin-6 overexpression induces pulmonary hypertension.Circulation research · 2009Article
- The cancer paradigm of severe pulmonary arterial hypertension.American journal of respiratory and critical care medicine · 2008Article
- Idiopathic pulmonary arterial hypertension.Disease models & mechanismsReview
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHuman pulmonary arterial hypertension (PAH) is characterized by proliferation of vascular smooth muscle and, in its more severe form, by the development of occlusive neointimal lesions. However, few animal models of pulmonary neointimal proliferation exist, thereby limiting a complete understanding of the pathobiology of PAH. Recent studies of the endothelin (ET) system demonstrate that deficiency of the ET(B) receptor predisposes adult rats to acute and chronic hypoxic PAH, yet these animals fail to develop neointimal lesions. Herein, we determined and thereafter showed that exposure of ET(B) receptor-deficient rats to the endothelial toxin monocrotaline (MCT) leads to the development of neointimal lesions that share hallmarks of human PAH. METHODS AND
resultsThe pulmonary hemodynamic and morphometric effects of 60 mg/kg MCT in control (MCT(+/+)) and ET(B) receptor-deficient (MCT(sl/sl)) rats at 6 weeks of age were assessed. MCT(sl/sl) rats developed more severe PAH, characterized by elevated pulmonary artery pressure, diminished cardiac output, and right ventricular hypertrophy. In MCT(sl/sl) rats, morphometric evaluation revealed the presence of neointimal lesions within small distal pulmonary arteries, increased medial wall thickness, and decreased arterial-to-alveolar ratio. In keeping with this, barium angiography revealed diminished distal pulmonary vasculature of MCT(sl/sl) rat lungs. Cells within neointimal lesions expressed smooth muscle and endothelial cell markers. Moreover, cells within neointimal lesions exhibited increased levels of proliferation and were located in a tissue microenvironment enriched with vascular endothelial growth factor, tenascin-C, and activated matrix metalloproteinase-9, factors already implicated in human PAH. Finally, assessment of steady state mRNA showed that whereas expression of ET(B) receptors was decreased in MCT(sl/sl) rat lungs, ET(A) receptor expression increased.
conclusionsDeficiency of the ET(B) receptor markedly accelerates the progression of PAH in rats treated with MCT and enhances the appearance of cellular and molecular markers associated with the pathobiology of PAH. Collectively, these results suggest an overall antiproliferative effect of the ET(B) receptor in pulmonary vascular homeostasis.
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