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Stretch-induced programmed myocyte cell death

W Cheng1, B Li, J Kajstura

  • 1Department of Medicine, New York Medical College, Valhalla 10595, USA.

The Journal of Clinical Investigation
|November 1, 1995
PubMed
Summary
This summary is machine-generated.

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Overstretching papillary muscles increases cell death and oxidant stress, impairing heart muscle function. A novel drug prevented these negative effects, suggesting a potential therapeutic target for cardiac overload.

Area of Science:

  • Cardiovascular Physiology
  • Cell Biology
  • Biomedical Engineering

Background:

  • Cardiac muscle overload can lead to detrimental cellular changes.
  • Understanding the molecular mechanisms of mechanical stress on myocytes is crucial for cardiac health.
  • Previous research suggests a link between mechanical load and cellular damage in the myocardium.

Purpose of the Study:

  • To investigate the impact of mechanical loading on myocyte cell death, oxidant stress, and force development.
  • To examine the role of Fas protein expression and myocyte slippage under overloaded conditions.
  • To evaluate the protective effects of a nitric oxide-releasing drug against mechanical stress-induced damage.

Main Methods:

  • Papillary muscles were subjected to two levels of mechanical loading (7-8 and 50 mN/mm2) for 3 hours.

Related Experiment Videos

  • Measurements included active/passive tensions, programmed cell death, superoxide anion formation, Fas expression, and myocyte slippage.
  • The effects of a nitric oxide-releasing drug (C87-3754) were assessed.

    • Main Results:

    • Overstretching significantly increased apoptotic myocyte and nonmyocyte cell death (21- and 2.4-fold, respectively).
    • Reactive oxygen species generation increased 2.4-fold, and Fas protein labeling increased 21-fold.
    • A 15% decrease in myocyte number within the muscle thickness, 7% decrease in sarcomere length, and impaired force maintenance were observed.

    Conclusions:

    • Myocardial overstretching is associated with oxidant stress, Fas expression, programmed cell death, and architectural changes.
    • These cellular events lead to impaired force development in overloaded cardiac muscle.
    • The nitric oxide-releasing drug effectively mitigated superoxide formation, cell death, and tension alterations, indicating therapeutic potential.