ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Inflammation, endothelial injury, and persistent pulmonary hypertension in heterozygous BMPR2-mutant mice.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 52 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
52 citing papers in PubMed, 99 citations in OpenAlex.
- A large animal model of heritable pulmonary arterial hypertension using BMPR2 gene-edited sheep.JCI insight · 2026Article
- A Large Animal Model of Heritable Pulmonary Arterial Hypertension Using Gene-editedbioRxiv : the preprint server for biology · 2026Article
- Perivascular inflammatory cells and their association with pulmonary arterial remodelling in dogs with pulmonary hypertension due to myxomatous mitral valve disease.Veterinary research communications · 2023Article
- Sotatercept analog suppresses inflammation to reverse experimental pulmonary arterial hypertension.Scientific reports · 2022Article
- The role of TGF-β or BMPR2 signaling pathway-related miRNA in pulmonary arterial hypertension and systemic sclerosis.Arthritis research & therapy · 2021Review
- Computational repurposing of therapeutic small molecules from cancer to pulmonary hypertension.Science advances · 2021Article
- Endothelial cells in the pathogenesis of pulmonary arterial hypertension.The European respiratory journal · 2021Review
- Impact of human immunodeficiency virus on pulmonary vascular disease.Global cardiology science & practice · 2021Review
- Endothelial-to-Mesenchymal Transition in Pulmonary Arterial Hypertension.Antioxidants & redox signaling · 2021Review
- Review
- A stroma-corrected ZEB1 transcriptional signature is inversely associated with antitumor immune activity in breast cancer.Scientific reports · 2019Article
- Silencing PDK1 limits hypoxia-induced pulmonary arterial hypertension in mice via the Akt/p70S6K signaling pathway.Experimental and therapeutic medicine · 2019Article
- Article
- Bone morphogenetic protein receptor signal transduction in human disease.The Journal of pathology · 2019Review
- NEDD9 targetsScience translational medicine · 2018Article
- TGF-β Signaling in Control of Cardiovascular Function.Cold Spring Harbor perspectives in biology · 2018Review
- Low dose monocrotaline causes a selective pulmonary vascular lesion in male and female pneumonectomized rats.Experimental lung research · 2018Article
- BMP type II receptor as a therapeutic target in pulmonary arterial hypertension.Cellular and molecular life sciences : CMLS · 2017Review
- Genotype-phenotype effects ofPulmonary circulation · 2016Article
- EETs Elicit Direct Increases in Pulmonary Arterial Pressure in Mice.American journal of hypertension · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Heterozygous bone morphogenetic protein receptor-II-knockout (BMPR2(+/-)) mice have a similar genetic trait like that in some idiopathic pulmonary arterial hypertension patients. To examine the effect of pulmonary endothelial injury in BMPR2(+/-) mice, we challenged the mice with two injections of monocrotaline combined with intratracheal instillation of replication-deficient adenovirus expressing 5-lipoxygenase (MCT+Ad5LO). After the challenge (1 wk), BMPR2(+/-) mice exhibited a doubling of right ventricular systolic pressure that was greater than that of wild-type mice and remained elevated for 3 wk before heart failure developed. Muscularization and thickening of small pulmonary arterioles was evident in the BMPR2(+/-) lungs at 2 wk after the challenge and became severe at 3 wk. Marked perivascular infiltration of T cells, B cells, and macrophages was associated with the remodeled vessels. Real-time PCR analysis showed that the expression of six endothelial cell markers in lung tissue was decreased to 20-40% of original levels at 1 wk after the challenge in both BMPR2(+/-) and wild-type mice and largely recovered in wild-type (50-80%) but not BMPR2(+/-) lungs (30-50%) at 3 wk after the challenge. Macrophage inflammatory protein-1alpha and fractalkine receptor expression doubled in BMPR2(+/-) compared with wild-type lungs. Expression of type I and type II BMP receptors, but not transforming growth factor-beta receptors, in the challenged BMPR2(+/-) and wild-type lungs showed a similar pattern of expression as that of endothelial markers. Apoptotic responses at 1 wk after MCT and Ad5LO challenge were also significantly greater in the BMPR2(+/-) lungs than the wild-type lungs. These data show that BMPR2(+/-) mice are more sensitive to MCT+Ad5LO-induced pulmonary hypertension than wild-type mice. Greater endothelial injury and an enhanced inflammatory response could be the underlying causes of the sensitivity and may work in concert with BMPR2 heterozygosity to promote the development of persistent pulmonary hypertension.
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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.