American journal of physical medicine & rehabilitation · 2001
Myofiber injury and regeneration in a canine homologue of Duchenne muscular dystrophy.
СтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
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Childers M K, Okamura C S, Bogan D J, Bogan J R, Sullivan M J, Kornegay J N
Аннотация
OBJECTIVE: To test the hypothesis that differential skeletal muscle involvement, previously observed in dogs with a homologue of Duchenne muscular dystrophy, correlates with the histochemical markers of myofiber injury and regeneration.
DESIGN: Evidence of injury (cellular penetration by Evans blue dye, immunoglobulin G expression, hematoxylin and eosin staining of necrotic figures), myofiber regeneration (fetal myosin heavy chain isoform expression), and morphologic indices in the cranial sartorius (CS), long digital extensor, and vastus lateralis muscles were examined in five dogs with dystrophy and five normal dogs.
RESULTS: Only the CS muscle, at 1 mo, demonstrated significant differences in injury when compared with age-matched controls. By 6 mo, the long digital extensor and vastus lateralis also suffered greater than normal injury. Only the dystrophic CS tissue expressed a notable increase in mean myofiber diameter when compared with other muscles at 6 mo. Normal CS muscles revealed a distinct population of small myofibers at this age.
CONCLUSION: The CS seems unique in its selective pathologic involvement. These differences may contribute to the marked regenerative response of this muscle in the dystrophic state. An improved understanding of mechanisms by which some dystrophin-deficient canine muscles remain spared from injury may provide clues to investigate and prevent the degenerative processes in humans.
DESIGN: Evidence of injury (cellular penetration by Evans blue dye, immunoglobulin G expression, hematoxylin and eosin staining of necrotic figures), myofiber regeneration (fetal myosin heavy chain isoform expression), and morphologic indices in the cranial sartorius (CS), long digital extensor, and vastus lateralis muscles were examined in five dogs with dystrophy and five normal dogs.
RESULTS: Only the CS muscle, at 1 mo, demonstrated significant differences in injury when compared with age-matched controls. By 6 mo, the long digital extensor and vastus lateralis also suffered greater than normal injury. Only the dystrophic CS tissue expressed a notable increase in mean myofiber diameter when compared with other muscles at 6 mo. Normal CS muscles revealed a distinct population of small myofibers at this age.
CONCLUSION: The CS seems unique in its selective pathologic involvement. These differences may contribute to the marked regenerative response of this muscle in the dystrophic state. An improved understanding of mechanisms by which some dystrophin-deficient canine muscles remain spared from injury may provide clues to investigate and prevent the degenerative processes in humans.