title: LCAT cholesterol esterification is associated with the increase of ApoE/ApoA-I ratio during atherosclerosis progression in rabbit.
abstract: Apolipoprotein A-I and Apolipoprotein E promote different steps of reverse cholesterol transport, including lecithin-cholesterol acyltransferase stimulation. Our aim was to study the changes in the levels of Apolipoprotein A-I, Apolipoprotein E, and lecithin-cholesterol acyltransferase activity during atherosclerosis progression in rabbits. Quantitative echocardiographic parameters were analyzed in order to evaluate, for the first time, whether atherosclerosis progression in rabbit is associated to apolipoproteins changes and alteration of indices of cardiac function, such as systolic strain and strain rate of the left ventricle. Atherosclerosis was induced by feeding rabbits for 8 weeks with 2 % cholesterol diet. The HDL levels of cholesterol and cholesteryl esters were measured by HPLC. The lecithin-cholesterol acyltransferase activity was evaluated both ex vivo, as cholesteryl esters/cholesterol molar ratio, and in vitro. Apolipoproteins levels were analyzed by ELISA. The HDL levels of cholesterol and cholesteryl esters increased, during treatment, up to 3.7- and 2.5-fold, respectively, compared to control animals. The lecithin-cholesterol acyltransferase activity in vitro was halved after 4 weeks. During cholesterol treatment, Apolipoprotein A-I level significantly decreased, whereas Apolipoprotein E concentration markedly increased. The molar ratio Apolipoprotein E/Apolipoprotein A-I was negatively correlated with the enzyme activity, and positively correlated with both increases in the intima-media thickness of common carotid wall and cardiac dysfunction signs, such as systolic strain and strain rate of the left ventricle.
authors.affiliation: Dipartimento delle Scienze Biologiche-Sezione di Fisiologia ed Igiene, Università di Napoli Federico II, via Mezzocannone 8, 80134 Naples, Italy.
authors.forename: Alessandro
authors.initials: A
authors.lastname: Carlucci
authors.forename: Luisa
authors.initials: L
authors.lastname: Cigliano
authors.forename: Bernardetta
authors.initials: B
authors.lastname: Maresca
authors.forename: Maria Stefania
authors.initials: MS
authors.lastname: Spagnuolo
authors.forename: Giovanni
authors.initials: G
authors.lastname: Di Salvo
authors.forename: Raffaele
authors.initials: R
authors.lastname: Calabrò
authors.forename: Paolo
authors.initials: P
authors.lastname: Abrescia
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000473:pathology; D016632:Apolipoprotein A-I / Q000097:blood*; D001057:Apolipoproteins E / Q000097:blood*; D050197:Atherosclerosis / Q000097:blood / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D002788:Cholesterol Esters / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood; D018450:Disease Progression; D004951:Esterification; D008297:Male; D009206:Myocardium / Q000473:pathology; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000097:blood*; D058226:Plaque, Atherosclerotic / Q000473:pathology; D011817:Rabbits; D013318:Stroke Volume; D017539:Tunica Intima / Q000473:pathology; D016276:Ventricular Function
chemical_list: D016632:Apolipoprotein A-I; D001057:Apolipoproteins E; D002788:Cholesterol Esters; D008076:Cholesterol, HDL; D007862:Phosphatidylcholine-Sterol O-Acyltransferase