Developmental changes of calcium transients and contractility during the cultivation of rat neonatal cardiomyocytes

Husse, Britta; Wussling, M

doi:10.1007/978-1-4613-1289-5_2

Cited by 12 publications

(18 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…RyR-mediated Ca 2ϩ release. A noticeable role of neonate RyRs has been implicated in numerous works conducted in a variety of experimental models, including multicellular preparations (1,16,25,28), primary cultures (12,14), and freshly isolated myocytes (9). Those studies have suggested based on the use of either ryanodine or caffeine, that the participation of RyRs in E-C coupling is sizeable in the neonate heart.…”

Section: Discussionmentioning

confidence: 98%

“…Acutely isolated myocytes and primary cultures have been experimental models typically used for developmental studies of E-C coupling (9,12,14). These models, however, present a number of inconveniences that hinder a precise quantification of the Ca 2ϩ flux that results from CICR.…”

Section: Discussionmentioning

confidence: 99%

“…For example, it has been reported that during the first day of postnatal life, ryanodine (0.1-1 M) decreases the systolic tension up to ϳ50% in multicellular preparations (1,16,25,28). In cultured neonate myocytes, ryanodine (0.1 M) reduced ϳ25% of the amplitude of intracellular Ca 2ϩ transients triggered by APs (12). In the same preparation, ryanodine (10 M) completely abolished spontaneous local Ca 2ϩ release events as well (14).…”

mentioning

confidence: 96%

See 2 more Smart Citations

Developmental changes of intracellular Ca²⁺transients in beating rat hearts

Escobar¹,

Ribeiro-Costa²,

Villalba-Galea³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Postnatal maturation of the rat heart is characterized by major changes in the mechanism of excitation-contraction (E-C) coupling. In the neonate, the t tubules and sarcoplasmic reticulum (SR) are not fully developed yet. Consequently, Ca(2+)-induced Ca(2+) release (CICR) does not play a central role in E-C coupling. In the neonate, most of the Ca(2+) that triggers contraction comes through the sarcolemma. In this work, we defined the contribution of the sarcolemmal Ca(2+) entry and the Ca(2+) released from the SR to the Ca(2+) transient during the first 3 wk of postnatal development. To this end, intracellular Ca(2+) transients were measured in whole hearts from neonate rats by using the pulsed local field fluorescence technique. To estimate the contribution of each Ca(2+) flux to the global intracellular Ca(2+) transient, different pharmacological agents were used. Ryanodine was applied to evaluate ryanodine receptor-mediated Ca(2+) release from the SR, nifedipine for dihydropyridine-sensitive L-type Ca(2+) current, Ni(2+) for the current resulting from the reverse-mode Na(+)/Ca(2+) exchange, and mibefradil for the T-type Ca(2+) current. Our results showed that the relative contribution of each Ca(2+) flux changes considerably during the first 3 wk of postnatal development. Early after birth (1-5 days), the sarcolemmal Ca(2+) flux predominates, whereas at 3 wk of age, CICR from the SR is the most important. This transition may reflect the progressive development of the t tube-SR units characteristic of mature myocytes. We have hence directly defined in the whole beating heart the developmental changes of E-C coupling previously evaluated in single (acutely isolated or cultured) cells and multicellular preparations.

show abstract

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 96%

See 1 more Smart Citation

Developmental changes of intracellular Ca²⁺transients in beating rat hearts

Escobar¹,

Ribeiro-Costa²,

Villalba-Galea³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…This maturation can be viewed histologically through the appearance of well-defined sarcomeres (Lucchesi and Sweadner, 1991), marked cardiomyocyte hypertrophy (Li et al, 1996) and cell binucleation (Soonpaa et al, 1996). In addition, the mechanisms of calcium handling are altered in maturing cardiomyocytes, with extracellular calcium current through membrane channels accounting for most of the calcium transient in embryonic and neonatal cardiomyocytes, and calcium release from internal sarcomeric stores accounting for the calcium transient of adult cardiomyocytes (Gomez et al, 1994; Husse and Wussling, 1996). This change in calcium handling is concurrent with an increase in expression of the sarcoplasmic/endoplasmic calcium ATPase (SERCA2a) and the Ryanodine receptor (RyR), which acts as the sarcomeric calcium release channel (Lodish et al, 2000).…”

Section: Cardiomyocyte Maturationmentioning

confidence: 99%

Mechanobiology of cardiomyocyte development

Jacot

Martin

Hunt

2010

Journal of Biomechanics

194

174

View full text Add to dashboard Cite

Cardiac cells are under constant, self-generated mechanical stress which can affect the differentiation of stem cells into cardiac myocytes, the development of differentiated cells and the maturation of cells in neonatal mammals. In this article, the effects of direct stretch, electrically induced beating and substrate elasticity on the behavior and development of cardiomyocytes are reviewed, with particular emphasis on the effects of substrate stiffness on cardiomyocyte maturation. In order to relate these observations to in-vivo mechanical conditions, we isolated the left ventricle of Black Swiss mice from embryonic day 13.5 through postnatal day 14 and measured the elastic modulus of the epicardium using atomic force microscope indentation. We found that the elastic modulus of the epicardium significantly changes at birth, from an embryonic value of 12 ± 4 kPa to a neonatal value of 39 ± 7 kPa. This change is in the range shown to significantly affect the development of neonatal cardiomyocytes.

show abstract

“…Therefore we used the closest available model of fetal myocardium at term : a primary culture of neonatal rat cardiomyocytes in which cells beat synchronously [13] and develop pacemaker activity [14]. Neonatal rat cardiomyocytes provide a unique in vitro model for studying the rhythm, intracellular calcium dynamics and cell-to-cell interactions of cardiomyocytes [15][16][17]. Cardiomyocytes can be grown as primary cultures of single cells, each with its own independent rate of contraction, or as a network of cells that beat synchronously.…”

Section: Introductionmentioning

confidence: 99%

The bile acid taurocholate impairs rat cardiomyocyte function: a proposed mechanism for intra-uterine fetal death in obstetric cholestasis

et al. 2001

View full text Add to dashboard Cite

Obstetric cholestasis is a liver disease of pregnancy that can be complicated by sudden, hitherto unexplained, intra-uterine fetal death. Because intra-uterine death occurs suddenly, and because fetal heart rate abnormalities have been reported in obstetric cholestasis, we hypothesized that intra-uterine death is caused by impaired fetal cardiomyocyte function, resulting in fetal cardiac arrest. Obstetric cholestasis is associated with raised levels of maternal and fetal serum bile acids, and we propose that these may alter cardiomyocyte function. It was not possible to investigate the effects of bile acids on the intact human fetal heart at a cellular level. Therefore we used the closest available model of fetal myocardium at term: a primary culture of neonatal rat cardiomyocytes in which cells beat synchronously and develop pacemaker activity. The effect of the primary bile acid taurocholate (0.3 mM and 3 mM) on cultures of single cardiomyocytes, each with its own independent rate of contraction, was a reversible decrease in the rate of contraction and in the proportion of beating cells (P < 0.001). Addition of taurocholate to a network of synchronously beating cells caused a similar decrease in the rate of contraction. Furthermore, the integrity of the network was destroyed, and cells ceased to beat synchronously. Taurocholate also resulted in altered calcium dynamics and loss of synchronous beating. These data suggest that raised levels of the bile acid taurocholate in the fetal serum in obstetric cholestasis may result in the development of a fetal dysrhythmia and in sudden intra-uterine death.

show abstract

Developmental changes of calcium transients and contractility during the cultivation of rat neonatal cardiomyocytes

Cited by 12 publications

References 18 publications

Developmental changes of intracellular Ca²⁺transients in beating rat hearts

Developmental changes of intracellular Ca²⁺transients in beating rat hearts

Mechanobiology of cardiomyocyte development

The bile acid taurocholate impairs rat cardiomyocyte function: a proposed mechanism for intra-uterine fetal death in obstetric cholestasis

Contact Info

Product

Resources

About

Developmental changes of calcium transients and contractility during the cultivation of rat neonatal cardiomyocytes

Cited by 12 publications

References 18 publications

Developmental changes of intracellular Ca2+transients in beating rat hearts

Developmental changes of intracellular Ca2+transients in beating rat hearts

Mechanobiology of cardiomyocyte development

The bile acid taurocholate impairs rat cardiomyocyte function: a proposed mechanism for intra-uterine fetal death in obstetric cholestasis

Contact Info

Product

Resources

About

Developmental changes of intracellular Ca²⁺transients in beating rat hearts

Developmental changes of intracellular Ca²⁺transients in beating rat hearts