Frontiers in Physiology (Jun 2016)

Ca2+-clock-dependent pacemaking in the sinus node is impaired in mice with a cardiac specific reduction in SERCA2 abundance

  • Sunil Jit Ramamoorthy Jeewanlal Logantha,
  • Mathis Korseberg Stokke,
  • Mathis Korseberg Stokke,
  • Mathis Korseberg Stokke,
  • Andrew J Atkinson,
  • Sanjay R Kharche,
  • Sajida eParveen,
  • Yawer eSaeed,
  • Ivar eSjaastad,
  • Ivar eSjaastad,
  • Ole M Sejersted,
  • Ole M Sejersted,
  • Halina eDobrzynski

DOI
https://doi.org/10.3389/fphys.2016.00197
Journal volume & issue
Vol. 7

Abstract

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Background: The sarcoplasmic reticulum Ca2+-ATPase (SERCA2) pump is an important component of the Ca2+-clock pacemaker mechanism that provides robustness and flexibility to sinus node pacemaking. We have developed transgenic mice with reduced cardiac SERCA2 abundance (Serca2 KO) as a model for investigating SERCA2’s role in sinus node pacemaking.Methods and Results: In Serca2 KO mice, ventricular SERCA2a protein content measured by Western blotting was 75% (P70% Serca2 downregulation.Conclusions: Serca2 KO mice show a disrupted Ca2+-clock-dependent pacemaker mechanism contributing to impaired sinus node and atrioventricular node function.

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