Journal
JOURNAL OF VASCULAR RESEARCH
Volume 53, Issue 3-4, Pages 149-162Publisher
KARGER
DOI: 10.1159/000448996
Keywords
Soluble endoglin; Endothelial dysfunction; Vascular contractility; Mice
Categories
Funding
- Czech Science Foundation GACR [GA15-24015S]
- Grant Agency of Charles University in Prague [1284214/C, 1158413C, SVV/2016/260293]
- European Regional Development Fund under the Innovative Economy Program of the European Union [POIG.01.01.02-00-069/09]
- Ministerio de Economia y Competitividad of Spain [SAF2013-43421-R, SAF2013-45784-R]
- Junta de Castilla y Leon [GR100]
- CIBERER
- Red de Investigacion Cooperativa en Enfermedades Renales (REDINREN) [RD12/0021/0032]
- European Regional Development Funds (FEDER)
- FEDER
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Aims: A soluble form of endoglin (sEng) was proposed to participate in the induction of endothelial dysfunction in small blood vessels. Here, we tested the hypothesis that high levels of sEng combined with a high-fat diet induce endothelial dysfunction in an atherosclerosis-prone aorta. Methods and Results: Six-month-old female and male transgenic mice overexpressing human sEng (Sol-Eng(+)) with low (Sol-Eng(+) low) or high (Sol-Eng(+) high) levels of plasma sEng were fed a high-fat rodent diet containing 1.25% cholesterol and 40% fat for 3 months. The plasma cholesterol and mouse sEng levels did not differ in the Sol-Eng(+) high and Sol-Eng(+) low mice. The expression of proinflammatory (P-selectin, ICAM-1, pNFkB and COX-2) and oxidative-stress-related markers (HO-1, NOX-1 and NOX-2) in the aortas of Sol-Eng(+) high female mice was significantly higher than in Sol-Eng(+) low female mice. Endothelium-dependent vasodilatation induced by acetylcholine was preserved better in the Sol-Eng(+) high female mice than in the Sol-Eng(+) low female mice. Conclusion: These results suggest that high concentrations of sEng in plasma in combination with a high-fat diet induce the simultaneous activation of proinflammatory, pro-oxidative and vasoprotective mechanisms in mice aorta and the balance of these biological processes determines whether the final endothelial phenotype is adaptive or maladaptive. (C) 2016 S. Karger AG, Basel
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