ArticleHypertension (Dallas, Tex. : 1979)2012
Role of the transcription factor erythroblastosis virus E26 oncogen homolog-1 (ETS-1) as mediator of the renal proinflammatory and profibrotic effects of angiotensin II.
Article in Hypertension (Dallas, Tex. : 1979), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 24 citations in OpenAlex.
- Autoantibodies Targeting ATInternational journal of molecular sciences · 2021Article
- Angiotensin II triggers RIPK3-MLKL-mediated necroptosis by activating the Fas/FasL signaling pathway in renal tubular cells.PloS one · 2020Article
- AT1 and AT2 receptors modulate renal tubular cell necroptosis in angiotensin II-infused renal injury mice.Scientific reports · 2019Article
- Angiotensin II-induced hypertension and cardiac hypertrophy are differentially mediated by TLR3- and TLR4-dependent pathways.American journal of physiology. Heart and circulatory physiology · 2019Article
- Ferritin Light Chain Confers Protection Against Sepsis-Induced Inflammation and Organ Injury.Frontiers in immunology · 2019Article
- Transcription Factor ETS-1 and Reactive Oxygen Species: Role in Vascular and Renal Injury.Antioxidants (Basel, Switzerland) · 2018Review
- Cutaneous exposure to lewisite causes acute kidney injury by invoking DNA damage and autophagic response.American journal of physiology. Renal physiology · 2018Article
- The pathogenesis of diclofenac induced immunoallergic hepatitis in a canine model of liver injury.Oncotarget · 2017Article
- Haploinsufficiency of the Transcription FactorJournal of the American Society of Nephrology : JASN · 2017Article
- A Transcriptional Regulatory Role for the Membrane Type-1 Matrix Metalloproteinase in Carcinogen-Induced Inflammasome Gene Expression.Gene regulation and systems biology · 2017Article
- Transcription factor avian erythroblastosis virus E26 oncogen homolog-1 is a novel mediator of renal injury in salt-sensitive hypertension.Hypertension (Dallas, Tex. : 1979) · 2015Article
- The transcription factor E26 transformation-specific sequence-1 mediates neointima formation in arteriovenous fistula.Journal of the American Society of Nephrology : JASN · 2014Article
- Krüppel-like factor 4 transcriptionally regulates TGF-β1 and contributes to cardiac myofibroblast differentiation.PloS one · 2013Article
- Article
- Genome-wide and candidate gene association studies of placental abruption.International journal of molecular epidemiology and genetics · 2013Article
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8 authors at 1 institution in 1 country.
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Abstract
Angiotensin II (Ang II) plays a major role in the pathogenesis of end-organ injury in hypertension via its diverse hemodynamic and nonhemodynamic effects. Erythroblastosis virus E26 oncogen homolog-1 (ETS-1) is an important transcription factor recently recognized as an important mediator of cell proliferation, inflammation, and fibrosis. In the present studies, we tested the hypothesis that ETS-1 is a common mediator of the renal proinflammatory and profibrotic effects of Ang II. C57BL6 mice (n=6 per group) were infused with vehicle (control), Ang II (1.4 mg/kg per day), Ang II and an ETS-1 dominant-negative peptide (10 mg/kg per day), or Ang II and an ETS-1 mutant peptide (10 mg/kg per day) via osmotic minipump for 2 or 4 weeks. The infusion of Ang II resulted in significant increases in blood pressure and left ventricular hypertrophy, which were not modified by ETS-1 blockade. The administration of ETS-1 dominant-negative peptide significantly attenuated Ang II-induced renal injury as assessed by urinary protein excretion, mesangial matrix expansion, and cell proliferation. Furthermore, ETS-1 dominant-negative peptide but not ETS-1 mutant peptide significantly reduced Ang II-mediated upregulation of transforming growth factor-β, connective tissue growth factor, and α-smooth muscle actin. In addition, ETS-1 blockade reduced several proinflammatory effects of Ang II, including macrophage infiltration, nitrotyrosine expression, and NOX4 mRNA expression. Our studies suggest that ETS-1 is a common mediator of the proinflammatory and profibrotic effects of Ang II-induced hypertensive renal damage and may result in the development of novel strategies in the treatment and prevention of end-organ injury in hypertension.
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