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Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells
08:32

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells

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Deferoxamine reduces and nitric oxide synthase inhibition increases neutrophil-mediated myotube injury

Thomas J McLoughlin1, Susan K Tsivitse, Jessica A Edwards

  • 1Skeletal Muscle Physiology Laboratory, The University of Toledo, Toledo, OH 43606, USA.

Cell and Tissue Research
|August 5, 2003
PubMed

Insights

Neutrophil-mediated skeletal muscle injury involves beta 2 integrin CD18 adhesion and iron-dependent hydroxyl radical production. Skeletal muscle nitric oxide synthase activity may protect against this neutrophil-induced damage.

Area of Science:

  • Biomedical Science
  • Muscle Physiology
  • Immunology

Background:

  • Neutrophil infiltration contributes to skeletal muscle injury.
  • The roles of reactive oxygen species (ROS), reactive nitrogen species (RNS), and beta 2 integrin CD18 in this process are not fully elucidated.

Purpose of the Study:

  • To investigate the specific contributions of ROS, RNS, and CD18 to neutrophil-induced myotube injury.
  • To determine the protective potential of nitric oxide synthase (NOS) activity in skeletal muscle.

Main Methods:

  • Human myotubes were co-cultured with human neutrophils.
  • Inhibitors targeting ROS, RNS, and CD18 were used.
  • Muscle injury was quantified using a (51)Cr release assay.

Main Results:

  • Catalase, deferoxamine (an iron chelator), and anti-CD18 antibody significantly reduced myotube injury.
  • Superoxide dismutase did not affect injury levels.
  • Inhibition of NOS increased myotube injury and decreased nitric oxide (NO) levels.

Conclusions:

  • Neutrophil-mediated skeletal muscle injury is primarily driven by CD18-mediated adhesion and iron-dependent hydroxyl radical generation.
  • Skeletal muscle NOS activity appears to confer protection against neutrophil-induced damage.

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