Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology · 2014
Mitochondrial adaptations during myocardial hypertrophy induced by abdominal aortic constriction.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Mei Zhusong, Wang Xinxing, Liu Weili, Gong Jingbo, Gao Xiujie, Zhang Tao, Xie Fang, Qian Lingjia
Аннотация
INTRODUCTION: 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.
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.