Endothelial to mesenchymal transition contributes to endothelial dysfunction in pulmonary arterial hypertension
Open accessAbstract
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by lung endothelial cell dysfunction and vascular remodeling. Normally, the endothelium forms an integral cellular barrier to regulate vascular homeostasis. During embryogenesis endothelial cells exhibit substantial plasticity that contribute to cardiac development by undergoing endothelial-to-mesenchymal transition (EndoMT). We determined the presence of EndoMT in the pulmonary vasculature in vivo and the functional effects on pulmonary artery endothelial cells (PAECs) undergoing EndoMT in vitro. Histologic assessment of patients with systemic sclerosis-associated PAH and the hypoxia/SU5416 mouse model identified the presence von Willebrand factor/α-smooth muscle actin-positive endothelial cells in up to 5% of pulmonary vessels. Induced EndoMT in PAECs by inflammatory cytokines IL-1β, tumor necrosis factor α, and transforming growth factor β led to actin cytoskeleton reorganization and the development of a mesenchymal morphology. Induced EndoMT cells exhibited up-regulation of mesenchymal markers, including collagen type I and α-smooth muscle actin, and a reduction in endothelial cell and junctional proteins, including von Willebrand factor, CD31, occludin, and vascular endothelial-cadherin. Induced EndoMT monolayers failed to form viable biological barriers and induced enhanced leak in co-culture with PAECs. Induced EndoMT cells secreted significantly elevated proinflammatory cytokines, including IL-6, IL-8, and tumor necrosis factor α, and supported higher immune transendothelial migration compared with PAECs. These findings suggest that EndoMT may contribute to the development of PAH.
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EndoMT has been linked to endothelial dysfunction as a cause for pulmonary arterial hypertension, a major complication in SSc.
“Furthermore, EndoMT has been linked to endothelial dysfunction as a cause for pulmonary arterial hypertension, a major complication in SSc (94).”
From Unraveling SSc Pathophysiology; The Myofibroblast (2018) · cites this paper as [94]
Endothelial cells that undergo EndoMT produce more IL-6, IL-8, and TNFα compared to normal endothelial cells.
“Notably, endothelial cells that undergo EndoMT produce more IL-6, IL-8 and TNFα compared to normal endothelial cells (94).”
From Unraveling SSc Pathophysiology; The Myofibroblast (2018) · cites this paper as [94]
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- Authors
- Good, R. B., Gilbane, A. J., Trinder, S. L., Denton, C. P., Coghlan, G., Abraham, D. J., & Holmes, A. M.
- Affiliations
- The Royal Free Hospital (GB)
- National Health Service (GB)
- Corresponding author
- Holmes, Alan M.
- ORCID
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 185
- Issue
- 7
- Pages
- 1850-1858
- ISSN
- 0002-9440 (ISSN-L)
- OpenAlex
- W2120187885
- Cited by
- 349
- References
- 47
- Citations by year
- 2026: 13 · 2025: 34 · 2024: 27 · 2023: 37 · 2022: 45 · 2021: 42 · 2020: 40 · 2019: 28 · 2018: 33 · 2017: 26 · 2016: 18 · 2015: 6
- FWCI
- 21.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed (publishedVersion)
- Open Research (University of Surrey) (submittedVersion)
- Surrey Research Insight Open Access (The University of Surrey) (submittedVersion)
- Funders
- The Nightingales Charitable Trust
- Arthritis Research UK
- Raynaulds and Scleroderma Association
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
- Health Sciences › Medicine › Pathology and Forensic Medicine › Systemic Sclerosis and Related Diseases
- Health Sciences › Medicine › Genetics › Vascular Anomalies and Treatments
- Keywords
- endothelial-to-mesenchymal transition, pulmonary arterial hypertension, endothelial dysfunction, pulmonary artery endothelial cells, vascular remodeling, systemic sclerosis-associated pulmonary arterial hypertension, inflammatory cytokines, actin cytoskeleton remodeling, endothelial barrier function, transendothelial migration, VE-cadherin, occludin
- MeSH terms
- Animals, Cells, Cultured, Endothelium, Humans, Hypertension, Pulmonary, Lung, Pulmonary Artery, Up-Regulation, Cytokines, Coculture Techniques, Endothelial Cells, Mice, Epithelial-Mesenchymal Transition, Vascular Remodeling
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