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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Tumor necrosis factor-alpha receptor 1 contributes to ethanol-induced vascular reactive oxygen species generation and hypertension

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Simplicio, Janaina A. [1, 2] ; Gonzaga, Natalia A. [1, 2] ; Nakashima, Marcelo A. [2] ; De Martinis, Bruno S. [3] ; Cunha, Thiago M. [1] ; Tirapelli, Luis F. [4] ; Tirapelli, Carlos R. [2]
Total Authors: 7
[1] Univ Sao Paulo, Fac Med Ribeirao Preto, Programa Posgrad Farmacol, Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Escola Enfermagem Ribeirao Preto, Lab Farmacol, Ave Bandeirantes 3900, BR-14040902 Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Preto, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Cirurgia & Anat, Ribeirao Preto, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: JOURNAL OF THE AMERICAN SOCIETY OF HYPERTENSION; v. 11, n. 10, p. 684-696, OCT 2017.
Web of Science Citations: 7

We evaluated the contribution of tumor necrosis factor-alpha receptor 1 (TNFR1) to ethanol-induced hypertension and vascular oxidative stress and the possible role of perivascular adipose tissue (PVAT) in such responses. Male C57BL/6 wild-type (WT) or TNFR1-deficient mice (TNFR1(-/-)) were treated with ethanol (20% vol/vol) for 12 weeks. Ethanol induced an increase in blood pressure in WT mice and TNFR1(-/-) at 4 and 5 weeks of treatment, respectively. Treatment with ethanol increased tumor necrosis factor-alpha and interleukin-6 levels in aortas with or without PVAT (PVAT+ and PVAT-, respectively) from WT mice, but not TNFR1(-/-). Ethanol increased superoxide anion (O-2(-)) generation, thiobarbituric acid reactive substance concentration, and the activity of superoxide dismutase and catalase in aortas (PVAT- and PVAT+) from WT mice, but not TNFR1(-/-). Conversely, ethanol consumption decreased the concentration of nitrate/nitrite in aortas (PVAT- and PVAT+) from WT mice, but not TNFR1(-/-). Treatment with ethanol increased myeloperoxidase activity in aortas (PVAT- and PVAT+) from WT mice, but not TNFR1(-/-). The major finding of our study is that TNFR1 contributes to ethanol-induced hypertension and oxidative stress in the vasculature. Additionally, TNFR1 plays a role in ethanol-induced increase in proinflammatory cytokines and neutrophils migration. However, PVAT does not counteract or aggravate the effects induced by ethanol. (C) 2017 American Society of Hypertension. All rights reserved. (AU)

FAPESP's process: 14/09595-0 - TNF-alpha participation in vascular dysfunction induced by chronic ethanol consumption: involvement of perivascular adipose tissue
Grantee:Janaina Aparecida Simplicio
Support type: Scholarships in Brazil - Doctorate