Abstract
Background. Severe burns result in hypercatabolic state and concomitant muscle atrophy that persists for several months, thereby limiting patient recovery. However, the effects of burns on the corresponding spinal dermatome remain unknown. This study aimed to investigate whether burns induce apoptosis of spinal cord ventral horn motor neurons (VHMNs) and consequently cause skeletal muscle wasting. Methods. Third-degree hindpaw burn injury with 1% total body surface area (TBSA) rats were euthanized 4 and 8 weeks after burn injury. The apoptosis profiles in the ventral horns of the lumbar spinal cords, sciatic nerves, and gastrocnemius muscles were examined. The Schwann cells in the sciatic nerve were marked with S100. The gastrocnemius muscles were harvested to measure the denervation atrophy. Result. The VHMNs apoptosis in the spinal cord was observed after inducing third-degree burns in the hindpaw. The S100 and TUNEL double-positive cells in the sciatic nerve increased significantly after the burn injury. Gastrocnemius muscle apoptosis and denervation atrophy area increased significantly after the burn injury. Conclusion. Local hindpaw burn induces apoptosis in VHMNs and Schwann cells in sciatic nerve, which causes corresponding gastrocnemius muscle denervation atrophy. Our results provided an animal model to evaluate burn-induced muscle wasting, and elucidate the underlying mechanisms.
Highlights
Severe burns are typically followed by a hypermetabolic state with increased proteolysis and lipolysis [1], which persists for at least 9 to 12 months after burns even after complete wound closure [2], thereby resulting in considerable erosion of the lean body mass, muscle weakness, and diminished capacity for complete rehabilitation
We suggested that third-degree burns could induce excessive autophagy activation, which contributes to muscle loss and apoptosis and is characterized by muscle denervation atrophy
Wu et al investigated the activation of the satellite cells following burn injuries and Merritt et al focused on the inflammatory and protein metabolism signaling responses of the skeletal muscles after burn injuries [29, 30]
Summary
Severe burns are typically followed by a hypermetabolic state with increased proteolysis and lipolysis [1], which persists for at least 9 to 12 months after burns even after complete wound closure [2], thereby resulting in considerable erosion of the lean body mass, muscle weakness, and diminished capacity for complete rehabilitation. Burn-induced nerve conduction deficits have been observed in 11% to 29% of patients with major burns, in older or critically ill patients [10]. These neuropathies cause skeletal muscle weakness and wasting [11], the underlying etiology of which remains unclear [12]. This study aimed to investigate whether burns induce apoptosis of spinal cord ventral horn motor neurons (VHMNs) and cause skeletal muscle wasting. Gastrocnemius muscle apoptosis and denervation atrophy area increased significantly after the burn injury. Local hindpaw burn induces apoptosis in VHMNs and Schwann cells in sciatic nerve, which causes corresponding gastrocnemius muscle denervation atrophy. Our results provided an animal model to evaluate burn-induced muscle wasting, and elucidate the underlying mechanisms
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