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Isolation, Culture, and Functional Characterization of Adult Mouse Cardiomyoctyes
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Isolation, Culture, and Functional Characterization of Adult Mouse Cardiomyoctyes

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The studies of cell damaging and cell growth factors which induce cardiomyopathy

H Kawaguchi1, M Shoki, H Sano

  • 1Department of Cardiovascular Medicine, Hokkaido University School of Medicine, Sapporo, Japan.

Japanese Circulation Journal
|October 1, 1992
PubMed

Insights

Phosphatidylinositide-specific phospholipase C (PLC) activity and inositol trisphosphate (IP3) production were elevated in cardiomyopathic hamster hearts. Sarcoplasmic reticulum (SR) calcium handling differed between models, potentially explaining myocyte death in BIO 53.58.

Area of Science:

  • Cardiovascular Research
  • Molecular Cardiology
  • Biochemistry

Background:

  • Phosphatidylinositide-specific phospholipase C (PLC) plays a role in cellular signaling.
  • Altered intracellular calcium handling is implicated in cardiomyopathies.
  • Angiotensinogen is a component of the renin-angiotensin system, found in the heart.

Purpose of the Study:

  • To investigate PLC activity and sarcoplasmic reticulum (SR) function in cardiomyopathic hamster models (BIO 14.6 and BIO 53.58) compared to controls (F1b).
  • To examine the expression and distribution of angiotensinogen in these hamster hearts.
  • To correlate biochemical findings with potential mechanisms of myocyte death.

Main Methods:

  • Measurement of PLC activity and inositol trisphosphate (IP3) production.
  • Assessment of sarcoplasmic reticulum (SR) calcium uptake and IP3-stimulated calcium release.
  • Analysis of angiotensinogen mRNA expression and immunohistochemical localization.

Main Results:

  • PLC activity and IP3 production were significantly higher in both cardiomyopathic hamster hearts (BIO 14.6 and BIO 53.58) compared to controls (F1b).
  • SR calcium uptake increased in BIO 14.6 but decreased in BIO 53.58. IP3-stimulated calcium release from SR increased in BIO 14.6 but decreased in BIO 53.58.
  • Angiotensinogen mRNA expression showed no difference between groups or with age. Immunohistochemistry revealed decreased angiotensinogen immunoreactivity in 20-week-old BIO 53.58 hamsters.

Conclusions:

  • Elevated PI response may lead to high intracellular calcium levels in cardiomyopathic myocytes.
  • Deterioration of SR function in BIO 53.58 hamsters, coupled with prolonged high intracellular calcium, may cause myocyte death.
  • Angiotensinogen expression and distribution are largely unaffected by cardiomyopathy or age in these models, suggesting its role in myocyte death is limited.

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