title: Association of uncoupling protein-2 expression with increased reactive oxygen species in residual myocardium of the enlarged left ventricle after myocardial infarction.
abstract: Left ventricular (LV) dilatation following myocardial infarction (MI) is a major determinant of the patient's prognosis, and myocardial energy metabolism may play a key role in LV remodeling. We aimed to investigate the relative timing of LV dilatation to LV function, myocardial energy regulation by uncoupling protein (UCP)-2, and cellular damage in the noninfarct zone. Myocardial infarction was produced in Sprague-Dawley rats by ligation of the coronary artery. The LV end-diastolic dimension (mm) increased (8.9+/-0.3 vs 6.8+/-0.8 in sham-operated rats, P<0.01) in association with elevation of the LV end-diastolic pressure (mmHg) (18+/-5 vs 6+/-2 in sham-operated rats) at 1 week following the ligation. At 4 weeks, the UCP-2 expression (180% of that in sham-operated rats) and LV end-diastolic dimension increased further (11.1+/-0.5, P<0.01) but there was no change in the LV end-diastolic pressure. The mechanisms for LV dilatation were quite different between the early and late stages after MI. In the late stage, augmentation of UCP-2 expression in the noninfarct zone may be related to the LV dilatation. Further examinations regarding the possibility of the protective role of UCP-2 are needed.
authors.affiliation: Second Department of Internal Medicine, School of Medicine, Kagawa University, Kagawa, Japan.
authors.forename: Peng
authors.initials: P
authors.lastname: Guo
authors.forename: Katsufumi
authors.initials: K
authors.lastname: Mizushige
authors.forename: Takahisa
authors.initials: T
authors.lastname: Noma
authors.forename: Kazushi
authors.initials: K
authors.lastname: Murakami
authors.forename: Tsunetatsu
authors.initials: T
authors.lastname: Namba
authors.forename: Makoto
authors.initials: M
authors.lastname: Ishizawa
authors.forename: Teppei
authors.initials: T
authors.lastname: Tsuji
authors.forename: Shoji
authors.initials: S
authors.lastname: Kimura
authors.forename: Masakazu
authors.initials: M
authors.lastname: Kohno
mesh_terms: D000818:Animals; D015152:Blotting, Northern; D004195:Disease Models, Animal; D004452:Echocardiography; D006439:Hemodynamics; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism*; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism*; D009203:Myocardial Infarction / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013997:Time Factors; D000071246:Uncoupling Protein 2; D015854:Up-Regulation; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D020257:Ventricular Remodeling
chemical_list: D007473:Ion Channels; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; C000604391:Ucp2 protein, rat; D000071246:Uncoupling Protein 2