Cell culture modifies Ca2+ signaling during excitation–contraction coupling in neonate cardiac myocytes

Snopko, Rose M.; Aromolaran, Ademuyiwa S.; Karko, Kimberly L.; Ramos-Franco, Josefina; Blatter, Lothar A.; Mejía-Alvarez, Rafael

doi:10.1016/j.ceca.2006.04.033

Cited by 25 publications

(31 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It has been reported that cultured myocytes from neonatal rats exhibit an apparent reduction of RyR density, and Ca 2+ signaling during E-C coupling is modified. 24 The present intact whole heart experiments may resolve these discrepancies due to the difference in methodology used. Our observation of the presence of functional SR in early embryonic stages is compatible with a recent report that SR begins to contribute significantly to E-C coupling by ED 11.5 in isolated embryonic mouse hearts, as determined using an optical mapping system.…”

Section: Contribution Of Serca To Relaxation In Fetal Ventricular Heartmentioning

confidence: 99%

“…23 In isolated myocytes, either cell -cell interactions or intact extracellular matrix is disturbed, and the effects of morphological changes of ventricular myoarchitecture on the diastolic function might be excluded from these investigations. Recently, an apparent reduction of RyR density has been reported in primary cultures, 24 indicating that SR function might be underestimated in cultures. Therefore, we designed the present study such that it was conducted using stimulated whole hearts to evaluate the developmental changes of Ca 2+ homeostasis under physiological conditions.…”

Section: + Transients In Immature Whole Heartsmentioning

confidence: 99%

“…It is possible, therefore, that the functional interaction between intrinsic cardiac adrenergic cells and cardiac myocytes in embryonic hearts, shown by the effect of a β-adrenergic blocker, 37 is modified in these single-cell models. Moreover, there are modifications in underlying β-adrenergic signaling pathways, 38 RyR density, 24 and E-C coupling that occur during cell cultivation. To eliminate all these factors, we conducted the present experiments using intact whole hearts of mouse embryos.…”

Section: Ca 2+ Transients In Whole Heart As Opposed To Single Myocytesmentioning

confidence: 99%

See 2 more Smart Citations

Fetal and Neonatal Development of Ca2+ Transients and Functional Sarcoplasmic Reticulum in Beating Mouse Hearts

Kawamura

Ishiwata

Takizawa

et al. 2010

Circ J

View full text Add to dashboard Cite

Background: It is generally accepted that Ca 2+ -induced Ca 2+ release is not the predominant mechanism during embryonic stages. Most studies have been conducted either on primary cultures or acutely isolated cells, in which an apparent reduction of ryanodine receptor density and alterations in the cell shape have been reported. The aim of the present study was to investigate developmental changes in Ca 2+ transients using whole hearts of mouse embryos and neonates. Methods and Results:Fluo-3 fluorescence signals from stimulated whole hearts were detected using a photomultiplier and stored as Ca 2+ transients. The upstroke and decay of Ca 2+ transients became more rapid from the late embryonic stages to the neonatal stage. After thapsigargin application (an inhibitor of the sarcoplasmic Ca 2+ -ATPase [SERCA]), time to 50% relaxation (T50) of Ca 2+ transients was significantly prolonged. There were no significant changes in T50 after Ru360 application (an inhibitor of mitochondrial Ca 2+ uniporter). The rate of increase in the amplitude of Ca 2+ transients after caffeine application became larger during developmental stages.Conclusions: Ca 2+ homeostasis developmentally changes from a slow rise and decay of Ca 2+ transients to rapid kinetics after the mid-embryonic stage. SERCA began to contribute significantly to Ca 2+ homeostasis at early embryonic stages and sarcoplasmic reticulum Ca 2+ contents increased from embryonic to neonatal stages, whereas mitochondrial Ca 2+ uptake did not contribute to Ca 2+ transients on a beat-to-beat basis. (Circ J 2010; 74: 1442 -1450

show abstract

Section: Contribution Of Serca To Relaxation In Fetal Ventricular Heartmentioning

confidence: 99%

Section: + Transients In Immature Whole Heartsmentioning

confidence: 99%

Section: Ca 2+ Transients In Whole Heart As Opposed To Single Myocytesmentioning

confidence: 99%

See 1 more Smart Citation

Fetal and Neonatal Development of Ca2+ Transients and Functional Sarcoplasmic Reticulum in Beating Mouse Hearts

Kawamura

Ishiwata

Takizawa

et al. 2010

Circ J

View full text Add to dashboard Cite

show abstract

“…However, a recent report demonstrated that RyR densities were reduced in cell culture, indicating that SR function might be underestimated in culture (16). Moreover, intrinsic cardiac adrenergic (ICA) cells play an important role in fetal heart development (34).…”

Section: Discussionmentioning

confidence: 99%

“…However, most of the studies have been conducted either on primary cultures or acutely isolated cells and an apparent reduction of RyR density (16) and alterations in cell shape (13) have been reported. Previously, we used fetal mouse whole heart models to examine the effect of a SR Ca 2ϩ ATPase inhibitor on this Ca 2ϩ transient and indicated that Ca 2ϩ reuptake from the SR might be functional even on embryonic day (ED) 12.5 (17).…”

mentioning

confidence: 99%

Contribution of Sarcoplasmic Reticulum Ca2+ Release and Ca2+ Transporters on Sarcolemmal Channels to Ca2+ Transient in Fetal Mouse Heart

et al. 2011

View full text Add to dashboard Cite

Sarcoplasmic reticulum (SR) Ca 2ϩ release has been shown not to be the predominant mechanism responsible for excitation-contraction (E-C) coupling in fetal myocytes. However, most of the studies have been conducted either on primary cultures or acutely isolated cells, in which an apparent reduction of ryanodine receptor density have been reported. We aimed to elucidate the contribution of SR Ca 2ϩ release and Ca 2ϩ transporters on sarcolemmal channels to Ca 2ϩ transients in fetal mouse whole hearts. On embryonic day 13.5, ryanodine significantly reduced the amplitude of the Ca 2ϩ transient to 27.2 Ϯ 4.4% of the control, and both nickel and SEA0400 significantly prolonged the time to peak from 84 Ϯ 2 ms to 140 Ϯ 5 ms and 129 Ϯ 6 ms, respectively, whereas nifedipine did not alter it. Therefore, at early fetal stages, SR Ca 2ϩ release should be an important component of E-C coupling, and T-type Ca 2ϩ channel and reverse mode sodium-calcium exchanger (NCX)-mediated SR Ca 2ϩ release could be the predominant contributors. Using embryonic mouse cultured cardiomyocytes, we showed that both nifedipine and nickel inhibited the ability of NCX to extrude Ca 2ϩ from the cytosol. From these results, we propose a novel idea concerning E-C coupling in immature heart. (Pediatr Res 69: 306-311, 2011)

show abstract

Ca-Homeostasis and Heart Failure: Focus on the Biophysics of Surface Membrane Ca-Fluxes

Banach

2013

Biophysics of the Failing Heart

View full text Add to dashboard Cite

Cell culture modifies Ca2+ signaling during excitation–contraction coupling in neonate cardiac myocytes

Cited by 25 publications

References 38 publications

Fetal and Neonatal Development of Ca2+ Transients and Functional Sarcoplasmic Reticulum in Beating Mouse Hearts

Fetal and Neonatal Development of Ca2+ Transients and Functional Sarcoplasmic Reticulum in Beating Mouse Hearts

Contribution of Sarcoplasmic Reticulum Ca2+ Release and Ca2+ Transporters on Sarcolemmal Channels to Ca2+ Transient in Fetal Mouse Heart

Ca-Homeostasis and Heart Failure: Focus on the Biophysics of Surface Membrane Ca-Fluxes

Contact Info

Product

Resources

About