ArticleAmerican journal of physiology. Lung cellular and molecular physiology2008
Pyrrolidine dithiocarbamate restores endothelial cell membrane integrity and attenuates monocrotaline-induced pulmonary artery hypertension.
Article in American journal of physiology. Lung cellular and molecular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 65 citations in OpenAlex.
- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- Important Functions and Molecular Mechanisms of Mitochondrial Redox Signaling in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2022Review
- Epigenetic Regulation of Endothelial Dysfunction and Inflammation in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2021Review
- Endothelial cells in the pathogenesis of pulmonary arterial hypertension.The European respiratory journal · 2021Review
- Rieske iron-sulfur protein induces FKBP12.6/RyR2 complex remodeling and subsequent pulmonary hypertension through NF-κB/cyclin D1 pathway.Nature communications · 2020Article
- Pulmonary Arterial Hypertension and Chronic Thromboembolic Pulmonary Hypertension: An Immunological Perspective.Journal of clinical medicine · 2020Review
- Article
- Upregulation of miR-335-3p by NF-κB Transcriptional Regulation Contributes to the Induction of Pulmonary Arterial Hypertension via APJ during Hypoxia.International journal of biological sciences · 2020Article
- The Search for Disease-Modifying Therapies in Pulmonary Hypertension.Journal of cardiovascular pharmacology and therapeutics · 2019Review
- Mechanisms contributing to persistently activated cell phenotypes in pulmonary hypertension.The Journal of physiology · 2019Review
- Enhanced caveolin-1 expression in smooth muscle cells: Possible prelude to neointima formation.World journal of cardiology · 2015Article
- Dexamethasone induces apoptosis in pulmonary arterial smooth muscle cells.Respiratory research · 2015Article
- The role of inflammation in hypoxic pulmonary hypertension: from cellular mechanisms to clinical phenotypes.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Nuclear factor κB inhibition reduces lung vascular lumen obliteration in severe pulmonary hypertension in rats.American journal of respiratory cell and molecular biology · 2014Article
- Pulmonary hypertension and metabolic syndrome: Possible connection, PPARγ and Caveolin-1.World journal of cardiology · 2014Review
- Reactive oxygen species and antioxidants in pulmonary hypertension.Antioxidants & redox signaling · 2013Review
- Nuclear factor κ-B is activated in the pulmonary vessels of patients with end-stage idiopathic pulmonary arterial hypertension.PloS one · 2013Article
- Associated inflammation or increased flow-mediated shear stress, but not pressure alone, disrupts endothelial caveolin-1 in infants with pulmonary hypertension.Pulmonary circulation · 2012Article
- STAT3 signaling in pulmonary arterial hypertension.JAK-STAT · 2012Review
- Activated CD47 promotes pulmonary arterial hypertension through targeting caveolin-1.Cardiovascular research · 2012Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Monocrotaline (MCT)-induced pulmonary artery hypertension (PAH) in rats is preceded by an inflammatory response, progressive endothelial cell membrane disruption, reduction in the expression of caveolin-1, and reciprocal activation of STAT3 (PY-STAT3). Superoxide and NF-kappaB have been implicated in PAH. To evaluate the role of caveolin-1, PY-STAT3 activation, and superoxide in PAH, MCT-injected rats were treated daily with pyrrolidine dithiocarbamate (PDTC; starting on days 1, 3, and 14 x 2 wk), an inhibitor of inflammation and NF-kappaB activation. Hemodynamic data, the expression of inhibitory (I)-kappaBalpha, caveolin-1, and Tie2 (a membrane protein), activation of PY-STAT3 and NF-kappaB, and superoxide chemiluminescence were examined. Rats developed progressive PAH at 2 wk post-MCT. There was progressive reduction in the expression of caveolin-1, Tie2, and activation of PY-STAT3 in the lungs. Reduction in I-kappaBalpha expression was present at 2 and 4 wk post-MCT. Superoxide chemiluminescence and NF-kappaB activation were observed only at 2 wk post-MCT and both decreased by 4 wk post-MCT despite progressive PAH. PDTC (starting on days 1 and 3) rescued caveolin-1 and Tie2, reversed MCT-induced PY-STAT3 activation, and attenuated PAH. In addition, PDTC restored I-kappaBalpha expression and reduced superoxide chemiluminescence at 2 wk but did not inhibit NF-kappaB activation despite attenuation of PAH. PDTC had no effect on established PAH. Increased superoxide chemiluminescence and NF-kappaB activation appear to be a transient phenomenon in the MCT model. Thus the disruption of endothelial cell membrane integrity resulting in caveolin-1 loss and reciprocal activation of PY-STAT3 plays a key role in the MCT-induced PAH.
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