ArticleCirculation research2012
Loss of adenomatous poliposis coli-α3 integrin interaction promotes endothelial apoptosis in mice and humans.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 33 citations in OpenAlex.
- Lung Pericytes: Molecular Mechanisms, Signaling Pathways, and Roles in Pulmonary Diseases.Comprehensive Physiology · 2026Review
- Loss of ROR2 Tyrosine Kinase Receptor Is Associated With Endothelial Dysfunction in PAH via Inappropriate Integrin β1 Activation.Hypertension (Dallas, Tex. : 1979) · 2026Article
- The emerging role of integrin signaling in pulmonary vascular disease.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Metabolic pathways, genomic alterations, and post-translational modifications in pulmonary hypertension and cancer as therapeutic targets and biomarkers.Frontiers in pharmacology · 2024Article
- Wnt7a deficit is associated with dysfunctional angiogenesis in pulmonary arterial hypertension.The European respiratory journal · 2023Article
- Dichotomous role of integrin-β5 in lung endothelial cells.Pulmonary circulation · 2022Article
- NovelFrontiers in medicine · 2021Article
- Intrinsic Endocardial Defects Contribute to Hypoplastic Left Heart Syndrome.Cell stem cell · 2020Article
- Frequent mutation of hypoxia-related genes in persistent pulmonary hypertension of the newborn.Respiratory research · 2020Article
- Loss of Endothelium-Derived Wnt5a Is Associated With Reduced Pericyte Recruitment and Small Vessel Loss in Pulmonary Arterial Hypertension.Circulation · 2019Article
- Elevated microRNA-135a is associated with pulmonary arterial hypertension in experimental mouse model.Oncotarget · 2017Article
- Patient-Specific iPSC-Derived Endothelial Cells Uncover Pathways that Protect against Pulmonary Hypertension in BMPR2 Mutation Carriers.Cell stem cell · 2017Article
- Induced Pluripotent Stem Cell Model of Pulmonary Arterial Hypertension Reveals Novel Gene Expression and Patient Specificity.American journal of respiratory and critical care medicine · 2017Article
- Translating Research into Improved Patient Care in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2017Review
- Increased Pyruvate Dehydrogenase Kinase 4 Expression in Lung Pericytes Is Associated with Reduced Endothelial-Pericyte Interactions and Small Vessel Loss in Pulmonary Arterial Hypertension.The American journal of pathology · 2016Article
- PDGF-dependent β-catenin activation is associated with abnormal pulmonary artery smooth muscle cell proliferation in pulmonary arterial hypertension.FEBS letters · 2016Article
- RNA Sequencing Analysis Detection of a Novel Pathway of Endothelial Dysfunction in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2015Article
- Targeting the Wnt signaling pathways in pulmonary arterial hypertension.Drug discovery today · 2014Review
- Whole-exome sequencing reveals TopBP1 as a novel gene in idiopathic pulmonary arterial hypertension.American journal of respiratory and critical care medicine · 2014Article
- Enhanced assay of endothelial exocytosis using extracellular matrix components.Analytical biochemistry · 2014Article
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Authors and funding
14 authors at 1 institution in 2 countries.
Funding
Abstract
rationalePulmonary hypertension (PH) is characterized by progressive elevation in pulmonary pressure and loss of small pulmonary arteries. As bone morphogenetic proteins promote pulmonary angiogenesis by recruiting the Wnt/β-catenin pathway, we proposed that β-catenin activation could reduce loss and induce regeneration of small pulmonary arteries (PAs) and attenuate PH.
objectiveThis study aims to establish the role of β-catenin in protecting the pulmonary endothelium and stimulating compensatory angiogenesis after injury. METHODS AND
resultsTo assess the impact of β-catenin activation on chronic hypoxia-induced PH, we used the adenomatous polyposis coli (Apc(Min/+)) mouse, where reduced APC causes constitutive β-catenin elevation. Surprisingly, hypoxic Apc(Min/+) mice displayed greater PH and small PA loss compared with control C57Bl6J littermates. PA endothelial cells isolated from Apc(Min/+) demonstrated reduced survival and angiogenic responses along with a profound reduction in adhesion to laminin. The mechanism involved failure of APC to interact with the cytoplasmic domain of the α3 integrin, to stabilize focal adhesions and activate integrin-linked kinase-1 and phospho Akt. We found that PA endothelial cells from lungs of patients with idiopathic PH have reduced APC expression, decreased adhesion to laminin, and impaired vascular tube formation. These defects were corrected in the cultured cells by transfection of APC.
conclusionsWe show that APC is integral to PA endothelial cells adhesion and survival and is reduced in PA endothelial cells from PH patient lungs. The data suggest that decreased APC may be a cause of increased risk or severity of PH in genetically susceptible individuals.
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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.