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The posterior cricoarytenoid muscle is spared from MuRF1-mediated muscle atrophy in mice with acute lung injury.

Publication ,  Journal Article
Files, DC; Xiao, K; Zhang, T; Liu, C; Qian, J; Zhao, W; Morris, PE; Delbono, O; Feng, X
Published in: PLoS One
2014

BACKGROUND: Skeletal muscle wasting in acute lung injury (ALI) patients increases the morbidity and mortality associated with this critical illness. The contribution of laryngeal muscle wasting to these outcomes is unknown, though voice impairments and aspiration are common in intensive care unit (ICU) survivors. We evaluated the intrinsic laryngeal abductor (PCA, posterior cricoarytenoid), adductor (CT, cricothyroid) and limb (EDL, extensor digitorum longus) muscles in a mouse model of ALI. METHODS: Escherichia coli lipopolysaccharides were instilled into the lungs of adult male C57Bl6J mice (ALI mice). Limb and intrinsic laryngeal muscles were analyzed for fiber size, type, protein expression and myosin heavy chain (MyHC) composition by SDS-PAGE and mass spectroscopy. RESULTS: Marked muscle atrophy occurred in the CT and EDL muscles, while the PCA was spared. The E3 ubiquitin ligase muscle ring finger-1 protein (MuRF1), a known mediator of limb muscle atrophy in this model, was upregulated in the CT and EDL, but not in the PCA. Genetic inhibition of MuRF1 protected the CT and EDL from ALI-induced muscle atrophy. MyHC-Extraocular (MyHC-EO) comprised 27% of the total MyHC in the PCA, distributed as hybrid fibers throughout 72% of PCA muscle fibers. CONCLUSION: The vocal cord abductor (PCA) contains a large proportion of fibers expressing MyHC-EO and is spared from muscle atrophy in ALI mice. The lack of MuRF1 expression in the PCA suggests a previously unrecognized mechanism whereby this muscle is spared from atrophy. Atrophy of the vocal cord adductor (CT) may contribute to the impaired voice and increased aspiration observed in ICU survivors. Further evaluation of the sparing of muscles involved in systemic wasting diseases may lead to potential therapeutic targets for these illnesses.

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Published In

PLoS One

DOI

EISSN

1932-6203

Publication Date

2014

Volume

9

Issue

1

Start / End Page

e87587

Location

United States

Related Subject Headings

  • Wasting Syndrome
  • Vocal Cords
  • Ubiquitin-Protein Ligases
  • Tripartite Motif Proteins
  • Muscular Atrophy
  • Muscle Proteins
  • Mice, Knockout
  • Mice
  • Male
  • Lipopolysaccharides
 

Citation

APA
Chicago
ICMJE
MLA
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Files, D. C., Xiao, K., Zhang, T., Liu, C., Qian, J., Zhao, W., … Feng, X. (2014). The posterior cricoarytenoid muscle is spared from MuRF1-mediated muscle atrophy in mice with acute lung injury. PLoS One, 9(1), e87587. https://doi.org/10.1371/journal.pone.0087587
Files, D Clark, Kunhong Xiao, Tan Zhang, Chun Liu, Jiang Qian, Weiling Zhao, Peter E. Morris, Osvaldo Delbono, and Xin Feng. “The posterior cricoarytenoid muscle is spared from MuRF1-mediated muscle atrophy in mice with acute lung injury.PLoS One 9, no. 1 (2014): e87587. https://doi.org/10.1371/journal.pone.0087587.
Files DC, Xiao K, Zhang T, Liu C, Qian J, Zhao W, et al. The posterior cricoarytenoid muscle is spared from MuRF1-mediated muscle atrophy in mice with acute lung injury. PLoS One. 2014;9(1):e87587.
Files, D. Clark, et al. “The posterior cricoarytenoid muscle is spared from MuRF1-mediated muscle atrophy in mice with acute lung injury.PLoS One, vol. 9, no. 1, 2014, p. e87587. Pubmed, doi:10.1371/journal.pone.0087587.
Files DC, Xiao K, Zhang T, Liu C, Qian J, Zhao W, Morris PE, Delbono O, Feng X. The posterior cricoarytenoid muscle is spared from MuRF1-mediated muscle atrophy in mice with acute lung injury. PLoS One. 2014;9(1):e87587.

Published In

PLoS One

DOI

EISSN

1932-6203

Publication Date

2014

Volume

9

Issue

1

Start / End Page

e87587

Location

United States

Related Subject Headings

  • Wasting Syndrome
  • Vocal Cords
  • Ubiquitin-Protein Ligases
  • Tripartite Motif Proteins
  • Muscular Atrophy
  • Muscle Proteins
  • Mice, Knockout
  • Mice
  • Male
  • Lipopolysaccharides