ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Compartment-specific expression of collagens and their processing enzymes in intrapulmonary arteries of IPAH patients.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
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- Transcriptional signatures of endothelial cells shape immune responses in cardiopulmonary health and disease.JCI insight · 2025Review
- Vascular Remodeling: The Multicellular Mechanisms of Pulmonary Hypertension.International journal of molecular sciences · 2025Review
- Adventitial fibroblasts direct smooth muscle cell-state transition in pulmonary vascular disease.eLife · 2025Article
- The Role of Hydrogen Sulfide in the Regulation of the Pulmonary Vasculature in Health and Disease.Antioxidants (Basel, Switzerland) · 2025Review
- A bovine model of hypoxia-induced pulmonary hypertension reveals a gradient of immune and matrisome response with a complement signature found in circulation.American journal of physiology. Cell physiology · 2024Article
- Proteomic Signatures of Right Ventricular Outcomes in Pulmonary Arterial Hypertension.Circulation. Heart failure · 2024Article
- Collagen 18A1/Endostatin Expression in the Progression of Right Ventricular Remodeling and Dysfunction in Pulmonary Arterial Hypertension.American journal of respiratory cell and molecular biology · 2024Article
- Circulating Biomarkers in Pulmonary Arterial Hypertension: An Update.Biomolecules · 2024Review
- Pentastatin, a matrikine of the collagen IVα5, is a novel endogenous mediator of pulmonary endothelial dysfunction.American journal of physiology. Cell physiology · 2023Article
- New insights into the natural history of bronchopulmonary dysplasia from proteomics and multiplexed immunohistochemistry.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- JMJD1C promotes smooth muscle cell proliferation by activating glycolysis in pulmonary arterial hypertension.Cell death discovery · 2023Article
- Tensions in Taxonomies: Current Understanding and Future Directions in the Pathobiologic Basis and Treatment of Group 1 and Group 3 Pulmonary Hypertension.Comprehensive Physiology · 2023Review
- Pericytes: The lung-forgotten cell type.Frontiers in physiology · 2023Review
- Aggrecan accumulates at sites of increased pulmonary arterial pressure in idiopathic pulmonary arterial hypertension.Pulmonary circulation · 2023Article
- Single-cell transcriptomics reveals skewed cellular communication and phenotypic shift in pulmonary artery remodeling.JCI insight · 2022Article
- Construction of a diagnostic signature and immune landscape of pulmonary arterial hypertension.Frontiers in cardiovascular medicine · 2022Article
- Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 3 countries.
Funding
Abstract
Alterations in extracellular matrix (ECM) have been implicated in the pathophysiology of pulmonary hypertension. Here, we have undertaken a compartment-specific study to elucidate the expression profile of collagens and their processing enzymes in donor and idiopathic pulmonary arterial hypertension (IPAH) pulmonary arteries. Predominant intimal, but also medial and perivascular, remodeling and reduced lumen diameter were detected in IPAH pulmonary arteries. Two-photon microscopy demonstrated accumulation of collagen fibers. Quantification of collagen in pulmonary arteries revealed collagen accumulation mainly in the intima of IPAH pulmonary arteries compared with donors. Laser capture-microdissected pulmonary artery profiles (intima+media and perivascular tissue) were analyzed by real-time PCR for ECM gene expression. In the intima+media of IPAH vessels, collagens (COL4A5, COL14A1, and COL18A1), matrix metalloproteinase (MMP) 19, and a disintegrin and metalloprotease (ADAM) 33 were higher expressed, whereas MMP10, ADAM17, TIMP1, and TIMP3 were less abundant. Localization of COLXVIII, its cleavage product endostatin, and MMP10, ADAM33, and TIMP1 was confirmed in pulmonary arteries by immunohistochemistry. ELISA for collagen XVIII/endostatin demonstrated significantly elevated plasma levels in IPAH patients compared with donors, whereas circulating MMP10, ADAM33, and TIMP1 levels were similar between the two groups. Endostatin levels were correlated with pulmonary arterial wedge pressure, and established prognostic markers of IPAH, right atrial pressure, cardiac index, 6-min walking distance, NH2-terminal pro-brain natriuretic peptide, and uric acid. Expression of unstudied collagens, MMPs, ADAMs, and TIMPs were found to be significantly altered in IPAH intima+media. Elevated levels of circulating collagen XVIII/endostatin are associated with markers of a poor prognosis.
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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.