Publication
Title
Angiotensin II increases coronary fibrosis, cardiac hypertrophy and the incidence of myocardial infarctions in mice
Author
Abstract
Objective: Apolipoprotein E deficient mice (ApoE-/-) with a heterozygous mutation in the fibrillin-1 gene (Fbn1C1039G+/-) develop increased arterial stiffness, accelerated plaque progression, spontaneous plaque ruptures, myocardial infarction (MI) and sudden death. In the present study we used angiotensin II (Ang II) infusion to assess the responsiveness of the ApoE-/-Fbn1C1039G+/-mouse model to risk factors of atherosclerosis, such as high blood pressure and inflammation. Methods and results: Osmotic minipumps filled with phosphate buffered saline or Ang II (1,000 ng/kg/day) were implanted in ApoE-/-Fbn1C1039G+/-mice at week 14 of Western diet (WD). After 4 weeks of therapy, we were not able to detect an increase in blood pressure, but we observed severe aneurysms in both the thoracic and abdominal aorta of Ang II treated mice. Plaque size and composition in the proximal ascending aorta was not altered. Nevertheless, coronary fibrosis, cardiac hypertrophy and a 6-fold increase in the occurrence of MI in Ang II-treated mice was observed, which did not result in a higher mortality. Conclusion: The study showed that Ang II treatment in ApoE-/-Fbn1C1039G+/-mice increased cardiac hypertrophy, coronary fibrosis and the incidence of MI, without affecting blood pressure, plaque vulnerability and survival.
Language
English
Source (journal)
Acta cardiologica. - Bruxelles
Publication
Bruxelles : 2016
ISSN
0001-5385
Volume/pages
71:4(2016), p. 483-488
ISI
000383816400014
Full text (Publisher's DOI)
Full text (open access)
UAntwerpen
Faculty/Department
Research group
Publication type
Subject
Affiliation
Publications with a UAntwerp address
External links
Web of Science
Record
Identification
Creation 03.10.2016
Last edited 09.06.2017
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