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Mechanical unloading of the heart activates the calpain system

Peter Razeghi1, Kaelin C Volpini, Mou-Er Wang

  • 1Department of Internal Medicine, Division of Cardiology, University of Texas Houston-Medical School, 6431 Fannin, MSB 1.222, Houston, TX 77030, USA.

Journal of Molecular and Cellular Cardiology
|October 10, 2006
PubMed

Insights

Mechanical unloading of the heart activates the calpain system, a key regulator of cardiomyocyte atrophy. Inhibition of calpain did not prevent cardiac atrophy, suggesting other pathways are involved.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • The mechanisms driving cardiomyocyte size reduction during mechanical unloading remain unclear.
  • The calpain system is implicated in regulating cardiomyocyte atrophy.

Purpose of the Study:

  • To investigate the role of the calpain system in cardiac atrophy due to mechanical unloading.
  • To assess the impact of calpain inhibition on cardiomyocyte size in unloaded hearts.

Main Methods:

  • Human failing heart samples were analyzed post-left ventricular assist device implantation and explantation.
  • Rodent hearts underwent heterotopic transplantation for mechanical unloading.
  • Calpain 1 and 2 expression, calpain activity, degradation products, and cardiomyocyte size were measured.
  • Calpain inhibition was studied in rodent hearts overexpressing calpastatin.

Main Results:

  • Mechanical unloading increased calpain 2 gene expression in human hearts.
  • Calpain 1 and 2 transcript levels, activity, and degradation products significantly increased in unloaded rat hearts.
  • Unexpectedly, cardiomyocyte size decreased even in hearts overexpressing calpastatin.

Conclusions:

  • Mechanical unloading activates the calpain system in mammalian hearts.
  • Calpain inhibition alone does not prevent cardiac atrophy, indicating the involvement of other proteolytic systems.

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