title: Western diet consumption promotes vascular remodeling in non-senescent mice consistent with accelerated senescence, but does not modify vascular morphology in senescent ones.
abstract: Senescence accelerated mice (SAM) are susceptible to developing vascular dysfunction and remodeling. Food intake and type of diet have also been identified as determining factors in vascular remodeling. However, the interplay between senescence and diet in vascular remodeling is largely unknown. We aimed to analyze structure of large (aorta) and small (mesenteric; MA) arteries from seven-month-old SAM prone (SAMP8) and resistant (SAMR1) mice that received a Western-type high-fat diet (WD; 8weeks). Aortic structure was assessed by morphometric analysis of hematoxylin and eosin-stained cross sections, and collagen content by qRT-PCR, immunofluorescence and picrosirius red. In MAs, structural and mechanical properties were measured by pressure myography; elastin and collagen content by qRT-PCR and immunofluorescence; nuclei distribution by confocal microscopy; and apoptosis by qRT-PCR and TUNEL assay. In aorta, wall thickness (WT), but not cross-sectional area (CSA), was increased by senescence, and WD only increased WT in SAMR1. WD intake, but not senescence, was associated with increased collagen deposition. In MAs, senescence diminished WT and CSA, without altering collagen and elastin deposition, reduced the number of MA wall cells, and increased pro apoptotic activation. WD consumption promoted in SAMR1 the same remodeling observed with senescence, while in SAMP8 the senescence-associated changes remained unaffected. The mechanisms involved in WD-induced MA remodeling in SAMR1 mimicked those observed in senescence per se. Our study reveals qualitatively different remodeling in aortas and MAs from senescent mice. Consumption of a WD induced remodeling of the SAMR1 vasculature similar to that induced by senescence, while it did not promote any further alteration in the latter. Therefore, we propose that increased consumption of fat-enriched diets could promote accelerated senescence of the non-senescent vasculature, although it does not exacerbate vascular remodeling during senescence.
authors.affiliation: Institut Clínic del Tòrax, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain.
authors.forename: Ana Paula
authors.initials: AP
authors.lastname: Dantas
authors.affiliation: Departament de Farmacologia, Terapèutica i Toxicologia, Institut de Neurociències, Facultat de Medicina, Universitat Autònoma de Barcelona (UAB), 08193 Bellaterra, Spain.
authors.forename: Yara
authors.initials: Y
authors.lastname: Onetti
authors.affiliation: Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, Av. Prof. Lineu Prestes, 1524, São Paulo, SP 05508-900, Brazil.
authors.forename: María Aparecida
authors.initials: MA
authors.lastname: Oliveira
authors.affiliation: Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, Av. Prof. Lineu Prestes, 1524, São Paulo, SP 05508-900, Brazil.
authors.forename: Maria Helena
authors.initials: MH
authors.lastname: Carvalho
authors.affiliation: Institut Clínic del Tòrax, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain.
authors.forename: Magda
authors.initials: M
authors.lastname: Heras
authors.affiliation: Departament de Farmacologia, Terapèutica i Toxicologia, Institut de Neurociències, Facultat de Medicina, Universitat Autònoma de Barcelona (UAB), 08193 Bellaterra, Spain.
authors.forename: Elisabet
authors.initials: E
authors.lastname: Vila
authors.affiliation: Departament de Farmacologia, Terapèutica i Toxicologia, Institut de Neurociències, Facultat de Medicina, Universitat Autònoma de Barcelona (UAB), 08193 Bellaterra, Spain. Electronic address: francesc.jimenez@uab.cat.
authors.forename: Francesc
authors.initials: F
authors.lastname: Jiménez-Altayó
mesh_terms: D000375:Aging / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D019588:Aging, Premature / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D000824:Animal Nutritional Physiological Phenomena / Q000502:physiology; D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D017209:Apoptosis / Q000502:physiology; D024042:Collagen Type I / Q000378:metabolism; D024061:Collagen Type III / Q000378:metabolism; D059305:Diet, High-Fat; D066273:Diet, Western; D005109:Extracellular Matrix / Q000378:metabolism; D005260:Female; D008638:Mesenteric Arteries / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D051379:Mice; D008815:Mice, Inbred Strains; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D066253:Vascular Remodeling / Q000502:physiology*
chemical_list: D024042:Collagen Type I; D024061:Collagen Type III
keywords: Apoptosis; Extracellular matrix; High-fat diet; Remodeling; Vascular senescence