Association of uncoupling protein-2 expression with increased reactive oxygen species in residual myocardium of the enlarged left ventricle after myocardial infarction

Heart Vessels. 2005 Mar;20(2):61-5. doi: 10.1007/s00380-004-0805-5.

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.

MeSH terms

  • Animals
  • Blotting, Northern
  • Disease Models, Animal
  • Echocardiography
  • Hemodynamics
  • Ion Channels / genetics
  • Ion Channels / metabolism*
  • Male
  • Mitochondria, Heart / metabolism
  • Mitochondrial Proteins / genetics
  • Mitochondrial Proteins / metabolism*
  • Myocardial Infarction / complications
  • Myocardial Infarction / metabolism*
  • Myocardial Infarction / physiopathology
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Oxidative Stress*
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Reactive Oxygen Species / metabolism*
  • Time Factors
  • Uncoupling Protein 2
  • Up-Regulation
  • Ventricular Dysfunction, Left / etiology
  • Ventricular Dysfunction, Left / metabolism*
  • Ventricular Dysfunction, Left / physiopathology
  • Ventricular Remodeling*

Substances

  • Ion Channels
  • Mitochondrial Proteins
  • RNA, Messenger
  • Reactive Oxygen Species
  • Ucp2 protein, rat
  • Uncoupling Protein 2