ArticleAmerican journal of physiology. Lung cellular and molecular physiology2008
Increased pulmonary vascular resistance and defective pulmonary artery filling in caveolin-1-/- mice.
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 59 papers.
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59 citing papers in PubMed, 88 citations in OpenAlex.
- CAVIN-2 positively correlates with diabetic PAD and promotes LDL transcytosis by inhibiting eNOS activation.Annals of medicine · 2025Article
- Defining the clinical validity of genes reported to cause pulmonary arterial hypertension.Genetics in medicine : official journal of the American College of Medical Genetics · 2023Article
- Schistosomiasis-associated pulmonary hypertension unveils disrupted murine gut-lung microbiome and reduced endoprotective Caveolin-1/BMPR2 expression.Frontiers in immunology · 2023Article
- Genes in pediatric pulmonary arterial hypertension and the most promisingFrontiers in genetics · 2022Review
- Endothelial pannexin 1-TRPV4 channel signaling lowers pulmonary arterial pressure in mice.eLife · 2021Article
- Ion channels as convergence points in the pathology of pulmonary arterial hypertension.Biochemical Society transactions · 2021Review
- Caveolar peroxynitrite formation impairs endothelial TRPV4 channels and elevates pulmonary arterial pressure in pulmonary hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Identifying Potential Mutations Responsible for Cases of Pulmonary Arterial Hypertension.The application of clinical genetics · 2021Review
- PV1 in Caveolae Controls Lung Endothelial Permeability.American journal of respiratory cell and molecular biology · 2020Article
- Physiologic Consequences of Caveolin-1 Ablation in Conventional Outflow Endothelia.Investigative ophthalmology & visual science · 2020Article
- Altered Lipid Domains Facilitate Enhanced Pulmonary Vasoconstriction after Chronic Hypoxia.American journal of respiratory cell and molecular biology · 2020Article
- The role of genomics and genetics in pulmonary arterial hypertension.Global cardiology science & practice · 2020Review
- Caveolin as a Novel Potential Therapeutic Target in Cardiac and Vascular Diseases: A Mini Review.Aging and disease · 2020Review
- Molecular genetic framework underlying pulmonary arterial hypertension.Nature reviews. Cardiology · 2020Review
- Expression of a Human Caveolin-1 Mutation in Mice Drives Inflammatory and Metabolic Defect-Associated Pulmonary Arterial Hypertension.Frontiers in medicine · 2020Article
- Injury-Induced Shedding of Extracellular Vesicles Depletes Endothelial Cells of Cav-1 (Caveolin-1) and Enables TGF-β (Transforming Growth Factor-β)-Dependent Pulmonary Arterial Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Downregulated caveolin-1 expression serves a potential role in coronary artery spasm by inducing nitric oxide productionExperimental and therapeutic medicine · 2018Article
- Reciprocal regulation of eNOS and caveolin-1 functions in endothelial cells.Molecular biology of the cell · 2018Article
- Angiogenic effects of apigenin on endothelial cells after hypoxia-reoxygenation via the caveolin-1 pathway.International journal of molecular medicine · 2017Article
- Genetics of Pulmonary Arterial Hypertension.Seminars in respiratory and critical care medicine · 2017Review
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7 authors at 1 institution in 1 country.
Funding
Abstract
Caveolin-1, the structural and signaling protein of caveolae, is an important negative regulator of endothelial nitric oxide synthase (eNOS). We observed that mice lacking caveolin-1 (Cav1(-/-)) had twofold increased plasma NO levels but developed pulmonary hypertension. We measured pulmonary vascular resistance (PVR) and assessed alterations in small pulmonary arteries to determine the basis of the hypertension. PVR was 46% greater in Cav1(-/-) mice than wild-type (WT), and increased PVR in Cav1(-/-) mice was attributed to precapillary sites. Treatment with NG-nitro-l-arginine methyl ester (l-NAME) to inhibit NOS activity raised PVR by 42% in WT but 82% in Cav1(-/-) mice, indicating greater NO-mediated pulmonary vasodilation in Cav1(-/-) mice compared with WT. Pulmonary vasculature of Cav1(-/-) mice was also less reactive to the vasoconstrictor thromboxane A2 mimetic (U-46619) compared with WT. We observed redistribution of type I collagen and expression of smooth muscle alpha-actin in lung parenchyma of Cav1(-/-) mice compared with WT suggestive of vascular remodeling. Fluorescent agarose casting also showed markedly decreased density of pulmonary arteries and artery filling defects in Cav1(-/-) mice. Scanning electron microscopy showed severely distorted and tortuous pulmonary precapillary vessels. Thus caveolin-1 null mice have elevated PVR that is attributed to remodeling of pulmonary precapillary vessels. The elevated basal plasma NO level in Cav1(-/-) mice compensates partly for the vascular structural abnormalities by promoting pulmonary vasodilation.
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