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Monitoring ER/SR Calcium Release with the Targeted Ca2+ Sensor CatchER+
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Published on: May 19, 2017

Calsequestrin mediates changes in spontaneous calcium release profiles.

Nessy Tania1, James P Keener

  • 1Department of Mathematics, University of Utah, 155 S. 1400 E. Room 233, Salt Lake City, UT 84112, USA. tania@math.utah.edu

Journal of Theoretical Biology
|July 23, 2010
PubMed
Summary

Calsequestrin (CSQ) regulates cardiac calcium release. Increasing CSQ enhances calcium sparks but reduces spontaneous release events by acting as both a buffer and a luminal sensor.

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Area of Science:

  • Cardiovascular Physiology
  • Molecular Cell Biology
  • Biophysics

Background:

  • Calsequestrin (CSQ) is the primary intracellular calcium buffer in cardiac sarcoplasmic reticulum (SR).
  • CSQ functions as a luminal sensor for Ryanodine receptors (RyRs), modulating calcium release.
  • Free, unbound CSQ desensitizes RyR channels to cytoplasmic calcium.

Purpose of the Study:

  • To investigate the dual role of CSQ as a calcium buffer and RyR luminal sensor.
  • To develop a minimal mechanistic model of the calcium release unit (CRU) incorporating CSQ dynamics.
  • To analyze the impact of altered CSQ expression on calcium release patterns and spontaneous release rates.

Main Methods:

  • Development of a mechanistic model for RyR-CSQ interactions.
  • Application of asymptotic approximations and mean first exit time calculations.
  • Derivation of a minimal CRU model with CSQ dependence.

Main Results:

  • Increased CSQ expression prolongs and enlarges calcium sparks due to buffering.
  • Elevated CSQ reduces basal spark rate and raises the SR calcium threshold for release termination via luminal sensing.
  • The CRU model demonstrates deterministic oscillations under high cytoplasmic calcium conditions.

Conclusions:

  • CSQ's dual function as a buffer and sensor significantly impacts cardiac calcium handling.
  • Modulating CSQ levels offers a potential mechanism to control calcium spark characteristics.
  • The developed model provides insights into the complex regulation of cardiac calcium release.