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Cyclic ADP-ribose does not affect cardiac or skeletal muscle ryanodine receptors

B R Fruen1, J R Mickelson, N H Shomer

  • 1Department of Veterinary PathoBiology, University of Minnesota, St. Paul 55108.

FEBS Letters
|September 26, 1994
PubMed

Insights

Cyclic ADP-ribose (cADPR) does not directly affect cardiac or skeletal ryanodine receptors (RYR). This study found no evidence that cADPR influences RYR activity in mammalian cardiac and skeletal muscle sarcoplasmic reticulum.

Area of Science:

  • Molecular biology
  • Cellular physiology
  • Biochemistry

Background:

  • The cardiac ryanodine receptor (RYR) is a calcium (Ca2+) release channel in mammalian cells.
  • Cyclic ADP-ribose (cADPR) has been proposed to target cardiac RYR channels.
  • Understanding RYR regulation is crucial for cardiac function.

Purpose of the Study:

  • To investigate the direct effect of cADPR on cardiac and skeletal muscle ryanodine receptor (RYR) activity.
  • To determine if cADPR modulates Ca2+ release through RYRs in mammalian muscle tissues.

Main Methods:

  • [3H]ryanodine binding assays on cardiac and skeletal muscle sarcoplasmic reticulum (SR) vesicles.
  • Single channel recordings of cardiac RYR activity in planar lipid bilayers.
  • Application of varying concentrations of cADPR, beta-NAD+, and ADP-ribose.

Main Results:

  • Neither cADPR, beta-NAD+, nor ADP-ribose affected [3H]ryanodine binding to cardiac SR vesicles.
  • cADPR did not activate single cardiac RYR channels in lipid bilayers.
  • cADPR did not affect skeletal muscle SR [3H]ryanodine binding.

Conclusions:

  • The findings argue against a direct role for cardiac and skeletal muscle RYRs in mediating cADPR-activated Ca2+ release.
  • This study challenges the proposed mechanism of cADPR action on well-characterized RYRs.
  • Further research is needed to elucidate the precise role of cADPR in cellular Ca2+ signaling.

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