title: Intrauterine growth restriction promotes vascular remodelling following carotid artery ligation in rats.
abstract: Epidemiological studies revealed an association between IUGR (intrauterine growth restriction) and an increased risk of developing CVDs (cardiovascular diseases), such as atherosclerosis or hypertension, in later life. Whether or not IUGR contributes to the development of atherosclerotic lesions, however, is unclear. We tested the hypothesis that IUGR aggravates experimentally induced vascular remodelling. IUGR was induced in rats by maternal protein restriction during pregnancy (8% protein diet). To detect possible differences in the development of vascular injury, a model of carotid artery ligation to induce vascular remodelling was applied in 8-week-old intrauterine-growth-restricted and control rat offspring. Histological and immunohistochemical analyses were performed in the ligated and non-ligated carotid arteries 8 weeks after ligation. IUGR alone neither caused overt histological changes nor significant dedifferentiation of VSMCs (vascular smooth muscle cells). After carotid artery ligation, however, neointima formation, media thickness and media/lumen ratio were significantly increased in rats after IUGR compared with controls. Moreover, dedifferentiation of VSMCs and collagen deposition in the media were more prominent in ligated carotids from rats after IUGR compared with ligated carotids from control rats. We conclude that IUGR aggravates atherosclerotic vascular remodelling induced by a second injury later in life.
authors.affiliation: Department of Pediatrics and Adolescent Medicine, University of Erlangen-Nürnberg, Erlangen, Germany. carlos.menendez-castro@uk-erlangen.de
authors.forename: Carlos
authors.initials: C
authors.lastname: Menendez-Castro
authors.forename: Nada
authors.initials: N
authors.lastname: Cordasic
authors.forename: Matthias
authors.initials: M
authors.lastname: Schmid
authors.forename: Fabian
authors.initials: F
authors.lastname: Fahlbusch
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Rascher
authors.forename: Kerstin
authors.initials: K
authors.lastname: Amann
authors.forename: Karl F
authors.initials: KF
authors.lastname: Hilgers
authors.forename: Andrea
authors.initials: A
authors.lastname: Hartner
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000473:pathology / Q000503:physiopathology*; D016893:Carotid Stenosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D054337:Cell Dedifferentiation / Q000502:physiology; D002454:Cell Differentiation / Q000502:physiology; D018753:Diet, Protein-Restricted; D004195:Disease Models, Animal; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D008026:Ligation; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000473:pathology / Q000503:physiopathology; D058426:Neointima / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar