title: The counter-regulatory effects of ESE-1 during angiotensin II-mediated vascular inflammation and remodeling.
abstract: 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.
authors.affiliation: Division of Cardiology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
authors.forename: Yumei
authors.initials: Y
authors.lastname: Zhan
authors.forename: Lei
authors.initials: L
authors.lastname: Yuan
authors.forename: Maiko
authors.initials: M
authors.lastname: Kondo
authors.forename: Peter
authors.initials: P
authors.lastname: Oettgen
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000503:physiopathology; D004268:DNA-Binding Proteins / Q000096:biosynthesis / Q000502:physiology*; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000139:chemically induced; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis; D014157:Transcription Factors / Q000096:biosynthesis / Q000502:physiology*; D014657:Vasculitis / Q000139:chemically induced / Q000503:physiopathology*
chemical_list: D004268:DNA-Binding Proteins; C494436:Elf3 protein, mouse; D014157:Transcription Factors; D000804:Angiotensin II; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse