Cardiac, skeletal, and smooth muscle mitochondrial respiration: are all mitochondria created equal?
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- Song-Young Park
- Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah;
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- Jayson R. Gifford
- Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah;
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- Robert H. I. Andtbacka
- Department of Surgery, Huntsman Cancer Hospital, University of Utah, Salt Lake City, Utah;
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- Joel D. Trinity
- Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah;
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- John R. Hyngstrom
- Department of Surgery, Huntsman Cancer Hospital, University of Utah, Salt Lake City, Utah;
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- Ryan S. Garten
- Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah;
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- Nikolaos A. Diakos
- Department of Internal Medicine, Division of Cardiovascular Medicine, University of Utah, Salt Lake City, Utah;
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- Stephen J. Ives
- Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah;
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- Flemming Dela
- Department of Biomedical Sciences, Copenhagen University, Copenhagen, Denmark; and
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- Steen Larsen
- Department of Biomedical Sciences, Copenhagen University, Copenhagen, Denmark; and
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- Stavros Drakos
- Department of Internal Medicine, Division of Cardiovascular Medicine, University of Utah, Salt Lake City, Utah;
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- Russell S. Richardson
- Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah;
説明
<jats:p>Unlike cardiac and skeletal muscle, little is known about vascular smooth muscle mitochondrial respiration. Therefore, the present study examined mitochondrial respiratory rates in smooth muscle of healthy human feed arteries and compared with that of healthy cardiac and skeletal muscles. Cardiac, skeletal, and smooth muscles were harvested from a total of 22 subjects (53 ± 6 yr), and mitochondrial respiration was assessed in permeabilized fibers. Complex I + II, state 3 respiration, an index of oxidative phosphorylation capacity, fell progressively from cardiac to skeletal to smooth muscles (54 ± 1, 39 ± 4, and 15 ± 1 pmol·s<jats:sup>−1</jats:sup>·mg<jats:sup>−1</jats:sup>, P < 0.05, respectively). Citrate synthase (CS) activity, an index of mitochondrial density, also fell progressively from cardiac to skeletal to smooth muscles (222 ± 13, 115 ± 2, and 48 ± 2 μmol·g<jats:sup>−1</jats:sup>·min<jats:sup>−1</jats:sup>, P < 0.05, respectively). Thus, when respiration rates were normalized by CS (respiration per mitochondrial content), oxidative phosphorylation capacity was no longer different between the three muscle types. Interestingly, complex I state 2 normalized for CS activity, an index of nonphosphorylating respiration per mitochondrial content, increased progressively from cardiac to skeletal to smooth muscles, such that the respiratory control ratio, state 3/state 2 respiration, fell progressively from cardiac to skeletal to smooth muscles (5.3 ± 0.7, 3.2 ± 0.4, and 1.6 ± 0.3 pmol·s<jats:sup>−1</jats:sup>·mg<jats:sup>−1</jats:sup>, P < 0.05, respectively). Thus, although oxidative phosphorylation capacity per mitochondrial content in cardiac, skeletal, and smooth muscles suggest all mitochondria are created equal, the contrasting respiratory control ratio and nonphosphorylating respiration highlight the existence of intrinsic functional differences between these muscle mitochondria. This likely influences the efficiency of oxidative phosphorylation and could potentially alter ROS production.</jats:p>
収録刊行物
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- American Journal of Physiology-Heart and Circulatory Physiology
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American Journal of Physiology-Heart and Circulatory Physiology 307 (3), H346-H352, 2014-08-01
American Physiological Society