Journal article
Apelin-13 treatment enhances the stability of atherosclerotic plaques.
- Fraga-Silva RA Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
- Seeman H Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Brazil.
- Montecucco F First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, Genoa, Italy.
- da Silva AR First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, Genoa, Italy.
- Burger F Division of Cardiology, Faculty of Medicine, Foundation for Medical Researches, University of Geneva, Geneva, Switzerland.
- Costa-Fraga FP Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
- Anguenot L Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
- Mach F Division of Cardiology, Faculty of Medicine, Foundation for Medical Researches, University of Geneva, Geneva, Switzerland.
- Dos Santos RAS Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Brazil.
- Stergiopulos N Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
- da Silva RF Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Brazil.
- 2018-01-17
Published in:
- European journal of clinical investigation. - 2018
APJ receptor
apelin
atherosclerosis
plaque stability
vulnerable plaque
Animals
Apelin
Carotid Artery Diseases
Collagen
Diet, Western
Lipid Metabolism
Lipids
Macrophages
Male
Mice, Inbred C57BL
Mice, Knockout, ApoE
Plaque, Atherosclerotic
Random Allocation
Reactive Oxygen Species
English
BACKGROUND
Apelin is an endogenous peptidergic system which modulates cardiovascular function. Recent studies pointed out a fundamental contribution of apelin on atherosclerosis development; however, such reports revealed contradictory data, and to date, it is difficult to accurately define a beneficial or deleterious role. To better understand apelin function on atherosclerosis, we aimed to investigate apelin-13 treatment effects on atherosclerotic plaques composition.
DESIGN
Apolipoprotein E gene-deleted mice were fed on Western-type diet for 11 weeks. Atherosclerotic plaque formation was induced in the carotid artery by a shear stress modifier device, which exposes the same vessel to distinct patterns of shear stress enabling the formation of plaques with different composition. Mice were treated with apelin-13 (2 mg kg-1 day-1 ) or vehicle for the last 3 weeks.
RESULTS
Apelin-13 treatment did not alter the lipid content of low shear stress- and oscillatory shear stress-induced plaques in the carotid. However, apelin-13 greatly ameliorated plaque stability by increasing intraplaque collagen content and reducing MMP-9 expression. Furthermore, apelin-13 decreased the infiltration of inflammatory cells (neutrophil and macrophage) and intraplaque reactive oxygen species content. Interestingly, apelin-13 treatment reduced total cholesterol, LDL levels and free fatty acid serum levels, while HDL, triglycerides serum levels were not significantly changed.
CONCLUSIONS
Apelin-13 treatment for 3 weeks did not alter the lesion size, but it significantly enhanced the stable phenotype of atherosclerotic plaques and improved serum lipid profile. These results indicate that activation of apelin system decreases plaque vulnerability.
Apelin is an endogenous peptidergic system which modulates cardiovascular function. Recent studies pointed out a fundamental contribution of apelin on atherosclerosis development; however, such reports revealed contradictory data, and to date, it is difficult to accurately define a beneficial or deleterious role. To better understand apelin function on atherosclerosis, we aimed to investigate apelin-13 treatment effects on atherosclerotic plaques composition.
DESIGN
Apolipoprotein E gene-deleted mice were fed on Western-type diet for 11 weeks. Atherosclerotic plaque formation was induced in the carotid artery by a shear stress modifier device, which exposes the same vessel to distinct patterns of shear stress enabling the formation of plaques with different composition. Mice were treated with apelin-13 (2 mg kg-1 day-1 ) or vehicle for the last 3 weeks.
RESULTS
Apelin-13 treatment did not alter the lipid content of low shear stress- and oscillatory shear stress-induced plaques in the carotid. However, apelin-13 greatly ameliorated plaque stability by increasing intraplaque collagen content and reducing MMP-9 expression. Furthermore, apelin-13 decreased the infiltration of inflammatory cells (neutrophil and macrophage) and intraplaque reactive oxygen species content. Interestingly, apelin-13 treatment reduced total cholesterol, LDL levels and free fatty acid serum levels, while HDL, triglycerides serum levels were not significantly changed.
CONCLUSIONS
Apelin-13 treatment for 3 weeks did not alter the lesion size, but it significantly enhanced the stable phenotype of atherosclerotic plaques and improved serum lipid profile. These results indicate that activation of apelin system decreases plaque vulnerability.
- Language
-
- English
- Open access status
- closed
- Identifiers
-
- DOI 10.1111/eci.12891
- PMID 29336478
- Persistent URL
- https://sonar.ch/global/documents/134336
Export to…
Statistics
Document views: 87
File downloads: