IMR Press / FBL / Volume 7 / Issue 4 / DOI: 10.2741/takeshim

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Intracellular Ca2+ store in embryonic cardiac myocytes

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1 Department of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi, Aoba-ku, Miyagi 980-8575, Japan
Academic Editor:Hector Valdivia
Front. Biosci. (Landmark Ed) 2002, 7(4), 1642–1652; https://doi.org/10.2741/takeshim
Published: 1 July 2002
(This article belongs to the Special Issue The structure and function of calcium release channels)
Abstract

In mature cardiac myocytes, Ca2+ influx through the L-type Ca2+ channel activates the ryanodine receptor and triggers Ca2+ release from the sarcoplasmic reticulum (SR). This Ca2+ signal amplification, termed Ca2+-induced Ca2+ release (CICR), occurs within the junctional membrane complex between the plasma membrane and the SR, and is essential for cardiac excitation-contraction (E-C) coupling. On the other hand, Ca2+ available during E-C coupling is predominantly derived from Ca2+ influx in embryonic cardiac myocytes. To examine the role of the intracellular Ca2+ store in immature cardiac myocytes, we have generated knockout mice lacking the cardiac type of the ryanodine receptor (RyR-2), or junctophilin (JP-2) contributing to formation of the junctional membrane complex. Both RyR-2- and JP-2-knockout mice show lethality at early embryonic stages immediately after beginning of heart beating. The loss of RyR-2 produced abnormal SR elements exhibiting vacuolated structures and Ca2+-overloading in embryonic cardiac myocytes. In JP-2-deficient cardiac myocytes, formation of junctional membrane complexes, called pheripheral couplings, was disturbed, and abnormal Ca2+ transients without spatial and temporal synchronization were observed. Therefore, the knockout mice have demonstrated that RyR-2-mediated Ca2+ release at the junctional membrane complex is essential for cellular Ca2+ homeostasis in immature cardiac myocytes.

Keywords
Intracellular Ca2+ Store
Junctophilin
Ryanodine Receptor
Sarcoplasmic Reticulum
Review
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