title: Mitochondrial adaptations during myocardial hypertrophy induced by abdominal aortic constriction.
abstract: BACKGROUND
  Myocardial hypertrophy is an adaptive response of the heart to work overload. Pathological cardiac hypertrophy is usually associated with the ultimate development of cardiac dysfunction and heart failure. The mitochondria have an important function in the development of cardiac hypertrophy. However, mitochondrial adaptations to hypertrophic stimulus remain ambiguous.
  
  
  METHODS
  A rat model of myocardial hypertrophy was established using abdominal aortic constriction. The expression of mitochondrial complexes was evaluated through electrophoresis using blue native and blue native/sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The enzyme activity of mitochondrial complexes was detected through in-gel activity.
  
  
  RESULTS
  Mitochondrial function and biogenesis decreased in hypertrophied myocardium. The content and activity of mitochondrial Complex V dimers and Complex I significantly decreased during hypertrophy, as well as those of the α, β, B, and D chains of the Complex V dimers. However, the content and activity of mitochondrial Complex V oligomers and Complexes II, III, and IV did not change.
  
  
  CONCLUSIONS
  The decreased content and activity of Complex V dimers and Complex I caused the decline in mitochondrial function and biogenesis during cardiac hypertrophy.
authors: Key laboratory of stress medicine, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, China, 100850.
authors: Zhusong
authors: Z
authors: Mei
authors: Key laboratory of stress medicine, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, China, 100850.
authors: Xinxing
authors: X
authors: Wang
authors: Key laboratory of stress medicine, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, China, 100850.
authors: Weili
authors: W
authors: Liu
authors: Key laboratory of stress medicine, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, China, 100850.
authors: Jingbo
authors: J
authors: Gong
authors: Key laboratory of stress medicine, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, China, 100850.
authors: Xiujie
authors: X
authors: Gao
authors: Key laboratory of stress medicine, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, China, 100850.
authors: Tao
authors: T
authors: Zhang
authors: Key laboratory of stress medicine, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, China, 100850.
authors: Fang
authors: F
authors: Xie
authors: Key laboratory of stress medicine, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, China, 100850. Electronic address: newjia@vip.sina.com.
authors: Lingjia
authors: L
authors: Qian
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001012:Aorta, Abdominal; D015153:Blotting, Western; D006332:Cardiomegaly / Q000378:metabolism* / Q000473:pathology*; D003251:Constriction, Pathologic; D004195:Disease Models, Animal; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D060888:Real-Time Polymerase Chain Reaction
keywords: Mitochondrial Complex V dimers; Mitochondrial Complex V oligomers; Mitochondrial dysfunction; Myocardial hypertrophy