Endothelial-to-mesenchymal transition drives atherosclerosis progression
The molecular mechanisms responsible for the development and progression of atherosclerotic lesions have not been fully established. Here, we investigated the role played by endothelial-to-mesenchymal transition (EndMT) and its key regulator FGF receptor 1 (FGFR1) in atherosclerosis. In cultured hum...
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| Published in | The Journal of clinical investigation Vol. 125; no. 12; pp. 4514 - 4528 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Society for Clinical Investigation
01.12.2015
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| Subjects | |
| Online Access | Get full text |
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| Abstract | The molecular mechanisms responsible for the development and progression of atherosclerotic lesions have not been fully established. Here, we investigated the role played by endothelial-to-mesenchymal transition (EndMT) and its key regulator FGF receptor 1 (FGFR1) in atherosclerosis. In cultured human endothelial cells, both inflammatory cytokines and oscillatory shear stress reduced endothelial FGFR1 expression and activated TGF-β signaling. We further explored the link between disrupted FGF endothelial signaling and progression of atherosclerosis by introducing endothelial-specific deletion of FGF receptor substrate 2 α (Frs2a) in atherosclerotic (Apoe(-/-)) mice. When placed on a high-fat diet, these double-knockout mice developed atherosclerosis at a much earlier time point compared with that their Apoe(-/-) counterparts, eventually demonstrating an 84% increase in total plaque burden. Moreover, these animals exhibited extensive development of EndMT, deposition of fibronectin, and increased neointima formation. Additionally, we conducted a molecular and morphometric examination of left main coronary arteries from 43 patients with various levels of coronary disease to assess the clinical relevance of these findings. The extent of coronary atherosclerosis in this patient set strongly correlated with loss of endothelial FGFR1 expression, activation of endothelial TGF-β signaling, and the extent of EndMT. These data demonstrate a link between loss of protective endothelial FGFR signaling, development of EndMT, and progression of atherosclerosis. |
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| AbstractList | The molecular mechanisms responsible for the development and progression of atherosclerotic lesions have not been fully established. Here, we investigated the role played by endothelial-to-mesenchymal transition (EndMT) and its key regulator FGF receptor 1 (FGFR1) in atherosclerosis. In cultured human endothelial cells, both inflammatory cytokines and oscillatory shear stress reduced endothelial FGFR1 expression and activated TGF-β signaling. We further explored the link between disrupted FGF endothelial signaling and progression of atherosclerosis by introducing endothelial-specific deletion of FGF receptor substrate 2 α (Frs2a) in atherosclerotic (Apoe(-/-)) mice. When placed on a high-fat diet, these double-knockout mice developed atherosclerosis at a much earlier time point compared with that their Apoe(-/-) counterparts, eventually demonstrating an 84% increase in total plaque burden. Moreover, these animals exhibited extensive development of EndMT, deposition of fibronectin, and increased neointima formation. Additionally, we conducted a molecular and morphometric examination of left main coronary arteries from 43 patients with various levels of coronary disease to assess the clinical relevance of these findings. The extent of coronary atherosclerosis in this patient set strongly correlated with loss of endothelial FGFR1 expression, activation of endothelial TGF-β signaling, and the extent of EndMT. These data demonstrate a link between loss of protective endothelial FGFR signaling, development of EndMT, and progression of atherosclerosis. In this paper, the authors investigated the role played by endothelial-to-mesenchymal transition (EndMT) and its key regulator FGF receptor 1 (FGFR1) in atherosclerosis. In cultured human endothelial cells, both inflammatory cytokines and oscillatory shear stress reduced endothelial FGFR1 expression and activated TGF-β signaling. They further explored the link between disrupted FGF endothelial signaling and progression of atherosclerosis by introducing endothelial-specific deletion of FGF receptor substrate 2 α (Frs2a) in atherosclerotic (Apoe^sup -/-^) mice. When placed on a high-fat diet, these double-knockout mice developed atherosclerosis at a much earlier time point compared with that their Apoe^sup -/-^ counterparts, eventually demonstrating an 84% increase in total plaque burden. Additionally, they conducted a molecular and morphometric examination of left main coronary arteries from 43 patients with various levels of coronary disease to assess the clinical relevance of these findings. These data demonstrate a link between loss of protective endothelial FGFR signaling, development of EndMT, and progression of atherosclerosis. In this paper, the authors investigated the role played by endothelial-to-mesenchymal transition (EndMT) and its key regulator FGF receptor 1 (FGFR1) in atherosclerosis. In cultured human endothelial cells, both inflammatory cytokines and oscillatory shear stress reduced endothelial FGFR1 expression and activated TGF- beta signaling. They further explored the link between disrupted FGF endothelial signaling and progression of atherosclerosis by introducing endothelial-specific deletion of FGF receptor substrate 2 alpha (Frs2a) in atherosclerotic (Apoe super( -/-)) mice. When placed on a high-fat diet, these double-knockout mice developed atherosclerosis at a much earlier time point compared with that their Apoe super( -/-) counterparts, eventually demonstrating an 84% increase in total plaque burden. Additionally, they conducted a molecular and morphometric examination of left main coronary arteries from 43 patients with various levels of coronary disease to assess the clinical relevance of these findings. These data demonstrate a link between loss of protective endothelial FGFR signaling, development of EndMT, and progression of atherosclerosis. The molecular mechanisms responsible for the development and progression of atherosclerotic lesions have not been fully established. Here, we investigated the role played by endothelial-to-mesenchymal transition (EndMT) and its key regulator FGF receptor 1 (FGFR1) in atherosclerosis. In cultured human endothelial cells, both inflammatory cytokines and oscillatory shear stress reduced endothelial FGFR1 expression and activated TGF-β signaling. We further explored the link between disrupted FGF endothelial signaling and progression of atherosclerosis by introducing endothelial-specific deletion of FGF receptor substrate 2α (Frs2α) in atherosclerotic ([Apoe.sup.-/-]) mice. When placed on a high-fat diet, these double-knockout mice developed atherosclerosis at a much earlier time point compared with that their [Apoe.sup.-/-] counterparts, eventually demonstrating an 84% increase in total plaque burden. Moreover, these animals exhibited extensive development of EndMT, deposition of fibronectin, and increased neointima formation. Additionally, we conducted a molecular and morphometric examination of left main coronary arteries from 43 patients with various levels of coronary disease to assess the clinical relevance of these findings. The extent of coronary atherosclerosis in this patient set strongly correlated with loss of endothelial FGFR1 expression, activation of endothelial TGF-β signaling, and the extent of EndMT. These data demonstrate a link between loss of protective endothelial FGFR signaling, development of EndMT, and progression of atherosclerosis. The molecular mechanisms responsible for the development and progression of atherosclerotic lesions have not been fully established. Here, we investigated the role played by endothelial-to-mesenchymal transition (EndMT) and its key regulator FGF receptor 1 (FGFR1) in atherosclerosis. In cultured human endothelial cells, both inflammatory cytokines and oscillatory shear stress reduced endothelial FGFR1 expression and activated TGF-β signaling. We further explored the link between disrupted FGF endothelial signaling and progression of atherosclerosis by introducing endothelial-specific deletion of FGF receptor substrate 2 α ( Frs2a ) in atherosclerotic ( Apoe –/– ) mice. When placed on a high-fat diet, these double-knockout mice developed atherosclerosis at a much earlier time point compared with that their Apoe –/– counterparts, eventually demonstrating an 84% increase in total plaque burden. Moreover, these animals exhibited extensive development of EndMT, deposition of fibronectin, and increased neointima formation. Additionally, we conducted a molecular and morphometric examination of left main coronary arteries from 43 patients with various levels of coronary disease to assess the clinical relevance of these findings. The extent of coronary atherosclerosis in this patient set strongly correlated with loss of endothelial FGFR1 expression, activation of endothelial TGF-β signaling, and the extent of EndMT. These data demonstrate a link between loss of protective endothelial FGFR signaling, development of EndMT, and progression of atherosclerosis. |
| Audience | Academic |
| Author | Chen, Pei-Yu Simons, Michael Qin, Lingfeng Baeyens, Nicolas Budatha, Madhusudhan Schwartz, Martin A. Li, Guangxin Tellides, George Afolabi, Titilayo |
| AuthorAffiliation | 2 Department of Surgery 4 Department of Biomedical Engineering, Yale University School of Medicine, New Haven, Connecticut, USA 1 Yale Cardiovascular Research Center, Department of Internal Medicine 3 Department of Cell Biology, and |
| AuthorAffiliation_xml | – name: 4 Department of Biomedical Engineering, Yale University School of Medicine, New Haven, Connecticut, USA – name: 2 Department of Surgery – name: 3 Department of Cell Biology, and – name: 1 Yale Cardiovascular Research Center, Department of Internal Medicine |
| Author_xml | – sequence: 1 givenname: Pei-Yu surname: Chen fullname: Chen, Pei-Yu – sequence: 2 givenname: Lingfeng surname: Qin fullname: Qin, Lingfeng – sequence: 3 givenname: Nicolas surname: Baeyens fullname: Baeyens, Nicolas – sequence: 4 givenname: Guangxin surname: Li fullname: Li, Guangxin – sequence: 5 givenname: Titilayo surname: Afolabi fullname: Afolabi, Titilayo – sequence: 6 givenname: Madhusudhan surname: Budatha fullname: Budatha, Madhusudhan – sequence: 7 givenname: George surname: Tellides fullname: Tellides, George – sequence: 8 givenname: Martin A. surname: Schwartz fullname: Schwartz, Martin A. – sequence: 9 givenname: Michael surname: Simons fullname: Simons, Michael |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26517696$$D View this record in MEDLINE/PubMed |
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| Snippet | The molecular mechanisms responsible for the development and progression of atherosclerotic lesions have not been fully established. Here, we investigated the... In this paper, the authors investigated the role played by endothelial-to-mesenchymal transition (EndMT) and its key regulator FGF receptor 1 (FGFR1) in... |
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| SubjectTerms | Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Animals Apolipoproteins E - genetics Apolipoproteins E - metabolism Atherosclerosis Biomechanics Biomedical research Collagen Coronary Artery Disease - genetics Coronary Artery Disease - metabolism Coronary Artery Disease - pathology Coronary vessels Cytokines Development and progression Fibroblast growth factor receptors Gene expression Genetic aspects Health aspects Heart attacks Human Umbilical Vein Endothelial Cells - metabolism Human Umbilical Vein Endothelial Cells - pathology Humans Hypertension Inflammation Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, Knockout Proteins Receptor, Fibroblast Growth Factor, Type 1 - genetics Receptor, Fibroblast Growth Factor, Type 1 - metabolism Shear stress Smooth muscle Software Studies Transforming Growth Factor beta - genetics Transforming Growth Factor beta - metabolism Veins & arteries |
| Title | Endothelial-to-mesenchymal transition drives atherosclerosis progression |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/26517696 https://www.proquest.com/docview/1746922347 https://www.proquest.com/docview/1728672851 https://www.proquest.com/docview/1765988254 https://pubmed.ncbi.nlm.nih.gov/PMC4665771 |
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