Endothelial Cells Expressing Endothelial and Mesenchymal Cell Gene Products in Lung Tissue From Patients With Systemic Sclerosis–Associated Interstitial Lung Disease
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Objective: To examine whether lung endothelial cells (ECs) from patients with systemic sclerosis (SSc)–associated interstitial lung disease (ILD) express mesenchymal cell–specific proteins and gene transcripts, indicative of the occurrence of endothelial‐to‐mesenchymal phenotypic transition (EndoMT). Methods: Lung tissue from 6 patients with SSc‐associated pulmonary fibrosis was examined by histopathology and immunohistochemistry. Confocal laser microscopy was utilized to assess the simultaneous expression of EC and myofibroblast molecular markers. CD31+CD102+ ECs were isolated from the lung tissue of 2 patients with SSc‐associated ILD and 2 normal control subjects, and the expression of EC and mesenchymal cell markers and other relevant genes was analyzed by quantitative polymerase chain reaction, immunofluorescence microscopy, and Western blotting. Results: Immunohistochemical staining revealed cells expressing the EC‐specific marker CD31 in the subendothelial, perivascular, and parenchymal regions of the lungs from all SSc patients. Confocal microscopy identified cells displaying simultaneous expression of von Willebrand factor and α‐smooth muscle actin in small and medium‐sized arterioles in the SSc lung tissue but not in normal control lungs. CD31+CD102+ ECs isolated from SSc lungs expressed high levels of mesenchymal cell–specific genes (type I collagen, type III collagen, and fibronectin), EC‐specific genes (type IV collagen and VE‐cadherin), profibrotic genes (transforming growth factor β1 and connective tissue growth factor), and genes encoding EndoMT‐related transcription factors (TWIST1 and SNAI2). Conclusion: Cells coexpressing EC‐ and mesenchymal cell–specific molecules are present in the lungs of patients with SSc‐associated ILD. CD31+CD102+ ECs isolated from SSc lungs simultaneously expressed mesenchymal cell– and EC‐specific transcripts and proteins. Collectively, these observations demonstrate the occurrence of EndoMT in the lungs of patients with SSc‐associated ILD.
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EndoMT can be identified using immunohistochemistry by observing endothelial cells with both endothelial markers (CD31, VE-cadherin) and myofibroblast markers (αSMA), and has been observed in skin and in lungs of SSc patients.
“EndoMT can be identified using immunohistochemistry by observing endothelial cells with both endothelial (cluster of differentiation (CD31, and VE-cadherin) and myofibroblast markers (αSMA), and has been observed in skin and in lungs of SSc patients (92, 93).”
From Unraveling SSc Pathophysiology; The Myofibroblast (2018) · cites this paper as [93]
Both EMT and EndoMT can be observed in SSc.
“Both processes can be observed in SSc.”
From Unraveling SSc Pathophysiology; The Myofibroblast (2018) · cites this paper as [93]
Two important sources of myofibroblasts in SSc are epithelial to mesenchymal transition (EMT) and endothelial to mesenchymal transition (EndoMT).
“Finally, two important sources of myofibroblasts in SSc are epithelial to mesenchymal transition (EMT) and endothelial to mesenchymal transition (EndoMT).”
From Unraveling SSc Pathophysiology; The Myofibroblast (2018) · cites this paper as [93]
In EMT and EndoMT, epithelial and endothelial cells lose their phenotype and become myofibroblasts.
“In both processes, respectively epithelial and endothelial cells lose their phenotype and become myofibroblasts.”
From Unraveling SSc Pathophysiology; The Myofibroblast (2018) · cites this paper as [93]
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- Authors
- Mendoza, F. A., Piera‐Velazquez, S., Farber, J. L., Feghali‐Bostwick, C., & Jiménez, S. A.
- Affiliations
- Thomas Jefferson University (US)
- Thomas Jefferson University Philadelphia Pennsylvania
- Medical University of South Carolina (US)
- Venue
- Arthritis & Rheumatology
- Publisher
- Wiley
- Published
- 2015-12-23
- Volume
- 68
- Issue
- 1
- Pages
- 210-217
- ISSN
- 2326-5191 (ISSN-L)
- 2326-5205
- PMC
- PMC4690777
- OpenAlex
- W2422507940
- Cited by
- 121
- References
- 43
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 9 · 2023: 9 · 2022: 9 · 2021: 17 · 2020: 14 · 2019: 12 · 2018: 10 · 2017: 17 · 2016: 9
- FWCI
- 9.53
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Arthritis & Rheumatology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- The Medicine Forum (submittedVersion)
- Funders
- NIH (National Institute of Arthritis and Musculoskeletal and Skin Diseases Core Center) (P30-AR-061271, K24-AR-060297, R01-AR-19616)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Systemic Sclerosis and Related Diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
- Keywords
- systemic sclerosis, interstitial lung disease, endothelial-to-mesenchymal transition, pulmonary endothelial cells, pulmonary fibrosis, myofibroblasts, CD31, TWIST1, SNAI2, TGF-β1, connective tissue growth factor, type I collagen, type III collagen, fibronectin, VE-cadherin, type IV collagen, von Willebrand factor, alpha-smooth muscle actin
- MeSH terms
- Snail Family Transcription Factors, Collagen Type I, alpha 1 Chain, Actins, Adult, Aged, Female, Fibronectins, Humans, Immunohistochemistry, Lung, Male, Middle Aged, Neovascularization, Pathologic, Nuclear Proteins, Scleroderma, Systemic, Transcription Factors, Blotting, Western, Lung Diseases, Interstitial, Microscopy, Confocal, Reverse Transcriptase Polymerase Chain Reaction, Collagen Type I, Collagen Type III, Endothelial Cells, Twist-Related Protein 1, Transforming Growth Factor beta1, Connective Tissue Growth Factor, Epithelial-Mesenchymal Transition
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