| The counter-regulatory effects of ESE-1 during angiotensin II-mediated vascular inflammation and remodeling. | |
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MedLine Citation:
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PMID: 20689519 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Angiotensin II (Ang II) is a critical mediator vascular inflammation and remodeling in a number of diseases including hypertension and atherosclerosis. The purpose of this study was to evaluate the role of the epithelium-specific ETS transcription factor-1 (ESE-1), a member of E26 transformation-specific sequence (ETS) transcription factors, as a mediator of Ang II-mediated vascular responses. METHODS: ESE-1 knockout mice were used to evaluate the role of ESE-1 in regulating Ang II-mediated vascular inflammation and remodeling. RESULTS: ESE-1 levels are low to undetectable under basal conditions but rapidly increase in response to Ang II. Intimal medial thickness and perivascular fibrosis of the aorta were significantly greater in ESE-1 knockout mice compared with the wild-type littermate controls. Proliferating cell nuclear antigen (PCNA) staining was also greater in the aorta of the Ang II-infused ESE-1 knockout mice compared with the controls. The infiltration of T cells and macrophage into the vessel wall of the aorta was dramatically enhanced in the ESE-1 knockout mice compared with the controls. Finally, Ang II-induced expression of a known downstream target of ESE-1, nitric oxide synthase 2 (NOS2), was significantly blunted in ESE-1 knockout mice compared to littermate controls. The alterations in vascular inflammation and remodeling were associated with an exaggerated systolic blood pressure response to Ang II in ESE-1 knockout mice. CONCLUSIONS: ESE-1 is an Ang II-inducible transcription factor that plays an important counter-regulatory role in the setting of vascular inflammation and remodeling. |
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Authors:
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Yumei Zhan; Lei Yuan; Maiko Kondo; Peter Oettgen |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2010-08-05 |
Journal Detail:
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Title: American journal of hypertension Volume: 23 ISSN: 1941-7225 ISO Abbreviation: Am. J. Hypertens. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-11-16 Completed Date: 2011-03-03 Revised Date: 2011-06-30 |
Medline Journal Info:
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Nlm Unique ID: 8803676 Medline TA: Am J Hypertens Country: United States |
Other Details:
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Languages: eng Pagination: 1312-7 Citation Subset: IM |
Affiliation:
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Division of Cardiology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA. |
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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pharmacology* Animals Aorta / drug effects, physiopathology DNA-Binding Proteins / biosynthesis, physiology* Endothelium, Vascular / metabolism Humans Hypertension / chemically induced Male Mice Mice, Knockout Nitric Oxide Synthase Type II / biosynthesis Transcription Factors / biosynthesis, physiology* Vasculitis / chemically induced, physiopathology* |
| Grant Support | |
ID/Acronym/Agency:
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R01-HL-67219/HL/NHLBI NIH HHS; R01-HL-82717/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/DNA-Binding Proteins; 0/Elf3 protein, mouse; 0/Transcription Factors; 11128-99-7/Angiotensin II; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nos2 protein, mouse |
| Comments/Corrections | |
Comment In:
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Am J Hypertens. 2010 Dec;23(12):1252
[PMID:
21079584
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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