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Am J Physiol Endocrinol Metab 279: E1114-E1121, 2000;
0193-1849/00 $5.00
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Vol. 279, Issue 5, E1114-E1121, November 2000

Skeletal muscle apoptosis after burns is associated with activation of proapoptotic signals

Shingo Yasuhara1, Mary-Ellen Perez1, Emi Kanakubo1, Yoko Yasuhara1, Yong-Sup Shin1, Masao Kaneki1, Toshiro Fujita2, and J. A. Jeevendra Martyn1

1 Department of Anesthesiology and Critical Care, Massachusetts General Hospital, Boston 02114, Shriners Burns Hospital, Boston 02114, and Harvard Medical School, Boston, Massachusetts 02115; and 2 Department of Internal Medicine, University of Tokyo, 112-0015 Tokyo, Japan

Critical illness is associated with muscle wasting and muscle weakness. Using burn injury as a model of local and systemic inflammatory response, we tested the hypothesis that thermal injury causes apoptosis in muscle. After a 40% body surface area burn to rats, abdominal muscles beneath the burn and limb muscles distant from the burn were examined for apoptosis at varying times after burn. Ladder assay, ELISA, and histological methods showed evidence of apoptosis in the abdominal muscles within 4-12 h with peak changes occurring at 3-7 days. Maximal apoptosis was also evident at distant limb muscles at 3-7 days. Investigation of proapoptotic pathways indicated mitochondrial membrane potential to be altered by 1 h after burn. Starting at 15 min after burn, cytochrome c was released from the mitochondria into the cytosol, followed by increased activity of caspase-3, starting at 6 h after burn. These studies suggest that mitochondria and caspase-mediated apoptotic pathways may be an additional mechanism of muscle weight loss in burns and may be potential therapeutic targets for prevention of muscle wasting.

muscle wasting; mitochondria; caspase; thermal injury


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