Contribution of Store-Operated Ca2+ Entry to Beat-to-Beat Ca2+ Transient in Early Fetal Mouse Heart

Introduction: Store-operated Ca2+ entry (SOCE) is triggered by ER/SR Ca2+ depletion to maintain intracellular Ca2+ concentration. In adult myocytes, SOCE contributes to cell growth or hypertrophy. However, in fetus, little is known about the role of SOCE. We hypothesize that SOCE may contribute to fetal cardiac contraction. Method: The whole hearts in embryonic day(ED) 9.5/12.5/15.5 and neonate were stained by Fluo-3 AM. Fluorescence signals in beating hearts stimulated electrically were recorded using a photomultiplier, then analyzed as Ca2+ transient(CaT) in each age. 1) SOCE was induced by changing the solutions from zero to 1.8mM Ca2+. With inhibiting voltage-dependent Ca2+ channels(VDCC), we tested whether SOCE was suppressed by 0.2mM Gd3+ application, as SOCE blocker. 2) We tested whether beat-to-beat CaT was suppressed by 0.2mM Gd3+ application. Results: 1) In fetal heart, SOCE was suppressed significantly by Gd3+ application (ED9.5; 46% decreased, p=0.011, n=5. ED12.5; 82% decreased, p<0.0001, n=6). 2) In ED 9.5, CaT was depressed significantly by Gd3+ application (49.2+/-7.6% vs. 2.0+/-2.0%), but after ED 12.5, CaT was not depressed. Conclusion: SOCE would contribute to beat-to-beat CaT in early fetal mouse myocytes.View Large Image | View Hi-Res Image | Download PowerPoint Slide