Intrinsic laryngeal muscles are spared from myonecrosis in the mdx mouse model of Duchenne muscular dystrophy

@article{Marques2007IntrinsicLM,
  title={Intrinsic laryngeal muscles are spared from myonecrosis in the mdx mouse model of Duchenne muscular dystrophy},
  author={Maria Julia Marques and Renato Ferretti and Viviane Urbini Vomero and Elaine Minatel and Humberto Santo Neto},
  journal={Muscle \& Nerve},
  year={2007},
  volume={35}
}
Intrinsic laryngeal muscles share many anatomical and physiological properties with extraocular muscles, which are unaffected in both Duchenne muscular dystrophy and mdx mice. We hypothesized that intrinsic laryngeal muscles are spared from myonecrosis in mdx mice and may serve as an additional tool to understand the mechanisms of muscle sparing in dystrophinopathy. Intrinsic laryngeal muscles and tibialis anterior (TA) muscle of adult and aged mdx and control C57Bl/10 mice were investigated… Expand
Dystrophic pathology in the intrinsic and extrinsic laryngeal muscles in the mdx mouse.
  • G. Smythe
  • Medicine
  • Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale
  • 2009
TLDR
With the exception of the cricothyroid, the intrinsic laryngeal muscles may be useful for comparison with the extraocular muscles to identify characteristics that spare them from disease pathology despite a dystrophin deficiency. Expand
Laryngeal muscles are spared in the dystrophin deficient mdx mouse.
TLDR
The authors concluded that these muscles are 1 of only a few muscle groups spared in this model of dystrophin deficiency, which highlights the unique aspects of the selected laryngeal skeletal muscles and their dissimilarity to limb skeletal muscle. Expand
Effect of dystrophin deficiency on selected intrinsic laryngeal muscles of the mdx mouse.
TLDR
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Differential levels of the calcium‐handling proteins may be involved in the pathogenesis of myonecrosis in mdx muscles, and understanding the signaling mechanisms involving Ca2+‐calmodulin activation and calsequestrin expression may be a valuable way to develop new therapeutic approaches to the dystrophinopaties. Expand
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Duchenne muscular dystrophy is due to genetic abnormalities in the dystrophin gene and represents one of the most frequent genetic childhood diseases. In the X-linked muscular dystrophy (mdx) mouseExpand
Muscle injury induced by different types of contractions in dystrophic mdx mice
TLDR
Both the lengthening and isometric contractions resulted in significantly greater injury to extensor digitorum longus muscles of mdx mice than to that of control mice, while the unloaded shortening contractions induce little injury to mdx muscles. Expand
Proteomic profiling of naturally protected extraocular muscles from the dystrophin-deficient mdx mouse.
TLDR
A comparative proteomic study of the established mdx mouse model of x-linked muscular dystrophy revealed a drastic up-regulation of utrophin, comparable levels of beta-dystroglycan and key Ca(2+)-regulatory elements, and an elevated concentration of small stress proteins in mdx extraocular muscles, suggesting that despite the lack of dystrophin only a limited number of cellular systems are perturbed in this naturally protected muscles. Expand
Laryngeal Findings in Duchenne Muscular Dystrophy.
TLDR
Patients with Duchene muscular dystrophy do not present abnormalities suggestive of the involvement of the intrinsic muscles of the larynx but have vocal worsening due to pulmonary impairment and there were no changes in muscular tone and mobility in the videolaryngoscopy. Expand
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TLDR
The mdx myopathy thus shows features seen in Duchenne muscular dystrophy, principally in that it exhibits a greater degree of compensatory muscle regeneration and an absence of fibro-fatty replacement of muscle fibres. Expand
Absence of extraocular muscle pathology in Duchenne's muscular dystrophy: role for calcium homeostasis in extraocular muscle sparing
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It is shown that dystrophin deficiency does not result in myonecrosis or pathologically elevated levels of intracellular calcium ([Ca2+]i) in EOM, and modulating levels of calcium homeostasis in muscle may be of potential therapeutic use in DMD. Expand
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It is proposed that careful investigation of the cellular determinants of extraocular muscle‐specific properties may provide insights into how these muscles avoid or adapt to the cascade of events leading to myofiber degeneration in the muscular dystrophies. Expand
mdx mice show progressive weakness and muscle deterioration with age
The time-course of degeneration/regeneration was investigated in leg muscles throughout the life of the mdx mutant mouse, which is a biochemical homologue of Duchenne muscular dystrophy (DMD). InExpand
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Significant myopathic changes including mitochondrial abnormalities develop in the thyrovocalis muscle with age and may play a role in the functional deficit of the larynx in old age. Expand
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It is concluded that CT and TA are distinct muscle allo-types and that laryngeal muscle fibers are subject to neural regulation. Expand
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Adult mouse intrinsic laryngeal muscles express high levels of the myogenic regulatory factor, MYF-5
TLDR
It is found that the adult thyroarytenoid muscles express much higher levels of both Myf-5 and EO-MyHC messenger ribonucleic acid (mRNA) compared to lower hindlimb skeletal muscle, suggesting that the unique functional characteristics of the intrinsic laryngeal muscles may be based in larynGEal muscle-specific gene expression directed by a unique combination of muscle regulatory factors. Expand
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