A computerized device for long-term measurements of the contraction frequency of cultured rat heart cells under stable incubating conditions

Rohr, Stephan

doi:10.1007/bf00370243

Cited by 14 publications

(11 citation statements)

References 18 publications

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“…3 As reported before for unstructured cardiomyocyte-myofibroblast cell monolayers, 33 discs of cardiomyocytes coated with myofibroblasts showed a characteristic transient increase of myofibroblast-dependent ectopic activity in response to the medium exchange ( Figure 7A). In preparations kept under control conditions, peak frequencies (+27%) were reached 1.7 hours following the medium exchange.…”

Section: Tgf-β 1 Affects Ectopic Activity In Models Of Cardiac Fibrosissupporting

confidence: 72%

TGF-β ₁ (Transforming Growth Factor-β ₁ ) Plays a Pivotal Role in Cardiac Myofibroblast Arrhythmogenicity

Salvarani

Maguy

Simone

et al. 2017

Circ: Arrhythmia and Electrophysiology

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Background-TGF-β 1 (transforming growth factor-β 1 ) importantly contributes to cardiac fibrosis by controlling differentiation, migration, and collagen secretion of cardiac myofibroblasts. It is still elusive, however, to which extent TGF-β 1 alters the electrophysiological phenotype of myofibroblasts and cardiomyocytes and whether it affects proarrhythmic myofibroblast-cardiomyocyte crosstalk observed in vitro. Methods and Results-Patch-clamp recordings of cultured neonatal rat ventricular myofibroblasts revealed that TGF-β 1 , applied for 24 to 48 hours at clinically relevant concentrations (≤2.5 ng/mL), causes substantial membrane depolarization concomitant with a several-fold increase of transmembrane currents. Transcriptome analysis revealed TGF-β 1 -dependent changes in 29 of 63 ion channel/pump/connexin transcripts, indicating a pleiotropic effect on the electrical phenotype of myofibroblasts. Whereas not affecting cardiomyocyte membrane potentials and cardiomyocyte-cardiomyocyte gap junctional coupling, TGF-β 1 depolarized cardiomyocytes coupled to myofibroblasts by ≈20 mV and increased gap junctional coupling between myofibroblasts and cardiomyocytes >5-fold as reflected by elevated connexin 43 and consortin transcripts. TGF-β 1 -dependent cardiomyocyte depolarization resulted from electrotonic crosstalk with myofibroblasts as demonstrated by immediate normalization of cardiomyocyte electrophysiology after targeted disruption of coupled myofibroblasts and by cessation of ectopic activity of cardiomyocytes coupled to myofibroblasts during pharmacological gap junctional uncoupling. In cardiac fibrosis models exhibiting slow conduction and ectopic activity, block of TGF-β 1 signaling completely abolished both arrhythmogenic conditions. Conclusions-TGF-β 1 profoundly alters the electrophysiological phenotype of cardiac myofibroblasts. Apart from possibly contributing to the control of cell function in general, the changes proved to be pivotal for proarrhythmic myofibroblastcardiomyocyte crosstalk in vitro, which suggests that TGF-β 1 may play a potentially important role in arrhythmogenesis of the fibrotic heart. (Circ Arrhythm Electrophysiol. 2017;10:e004567.

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Section: Tgf-β 1 Affects Ectopic Activity In Models Of Cardiac Fibrosissupporting

confidence: 72%

TGF-β ₁ (Transforming Growth Factor-β ₁ ) Plays a Pivotal Role in Cardiac Myofibroblast Arrhythmogenicity

Salvarani

Maguy

Simone

et al. 2017

Circ: Arrhythmia and Electrophysiology

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“…19,20 The presence of focal pacemaking regions in dense monolayer cultures of cultured cardiomyocytes has recently been verified experimentally in monolayer cultures. 21 In contrast to previous studies, which found spontaneous activity to be a ubiquitous phenomenon in monolayer cultures of cardiomyocytes, 14 the preparations used in the present study were generally only active after enhancing L-type Ca 2ϩ currents with BayK8644. This is in accordance with an earlier study showing a Ca 2ϩ current dependence of the pacemaking mechanism in these preparations.…”

Section: Spontaneous Activity In Monolayer Cultures Of Cardiomyocytescontrasting

confidence: 65%

Power-Law Behavior of Beat-Rate Variability in Monolayer Cultures of Neonatal Rat Ventricular Myocytes

Kučera

Heuschkel

Renaud

et al. 2000

Circulation Research

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Abstract-It is known that extracardiac factors (nervous, humoral, and hemodynamic) participate in the power-law behavior of heart-rate variability. To assess whether intrinsic properties of cardiac tissue might also be involved, beat-rate variability was studied in spontaneously beating cell cultures devoid of extracardiac influences. Extracellular electrograms were recorded from monolayer cultures of neonatal rat ventricular myocytes under stable incubating conditions for up to 9 hours. The beat-rate time series of these recordings were examined in terms of their Fourier spectra and their Hurst scaling exponents. A non-0 Hurst exponent was found in 21 of 22 preparations (0.29Ϯ0.09; range, 0.11 to 0.45), indicating the presence of fractal self-similarity in the beat-rate time series. The same preparations exhibited power-law behavior of the power spectra with a power-law exponent of Ϫ1.36Ϯ0.24 (range, Ϫ1.04 to Ϫ1.96) in the frequency range of 0.001 to 1 Hz. Furthermore, it was found that the power-law exponent was nonstationary over time. These results indicate that the power-law behavior of heart-rate variability is determined not only by extracardiac influences but also by components intrinsic to cardiac tissue. Furthermore, the presence of power-law behavior in monolayer cultures of cardiomyocytes suggests that beat-rate variability might be determined by the complex nonlinear dynamics of processes occurring at the level of the cellular network, eg, interactions among a large number of cell oscillators or metabolic regulatory systems. (Circ Res. 2000;86:1140-1145.)Key Words: heart-rate variability Ⅲ cardiac cell cultures Ⅲ physiology Ⅲ extracellular recording B eat-to-beat variations in cardiac cycle length have received increasing attention, because their characteristics may be used for the assessment and follow-up of various cardiovascular derangements and for risk stratification in the course of cardiac disease, including prediction of arrhythmias in cardiac patients. 1,2 Spectral analysis of beat-rate time series reveals periodic components in heart-rate variability (HRV). 3 In humans, 2 major components are present at frequencies around 0.1 Hz (low-frequency [LF] component) and around 0.25 Hz (highfrequency [HF] component). 4 It is well established that these periodic components are linked to breathing and blood pressure control and that they are mediated by the autonomic nervous system 5,6 and by endocrine influences. 3 However, the analysis of long-term recordings (ie, 24-hour Holter electrocardiograms) indicates that Ͼ95% of the spectral power of HRV is concentrated at frequencies below LF. 1 At these very low frequencies, the spectrum follows a power-law behavior; ie, the intensity of the power spectrum is a power function of frequency. The exponent of this power-law is close to Ϫ1 in healthy human subjects. 7 Several studies showed that this exponent is different after myocardial infarction 8,9 or cardiac transplantation 9 and that the characterization of power-law behavior can yield potent estimate...

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“…To measure the cycle-length distribution, we obtained the power spectra by Fourier transformation (FT), rather than by defining an arbitrary intensity level and measuring the duration from activation to activation as has been done in previous studies (28). Both methods lead to comparable results but exhibit pros and cons.…”

Section: Resultsmentioning

confidence: 99%

Rigidity Matching between Cells and the Extracellular Matrix Leads to the Stabilization of Cardiac Conduction

Hörning

Kidoaki

Kawano

et al. 2012

Biophysical Journal

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Biomechanical dynamic interactions between cells and the extracellular environment dynamically regulate physiological tissue behavior in living organisms, such as that seen in tissue maintenance and remodeling. In this study, the substrate-induced modulation of synchronized beating in cultured cardiomyocyte tissue was systematically characterized on elasticity-tunable substrates to elucidate the effect of biomechanical coupling. We found that myocardial conduction is significantly promoted when the rigidity of the cell culture environment matches that of the cardiac cells (4 kiloPascals). The stability of spontaneous target wave activity and calcium transient alternans in high frequency-paced tissue were both enhanced when the cell substrate and cell tissue showed the same rigidity. By adapting a simple theoretical model, we reproduced the experimental trend on the rigidity matching for the synchronized excitation. We conclude that rigidity matching in cell-to-substrate interactions critically improves cardiomyocyte-tissue synchronization, suggesting that mechanical coupling plays an essential role in the dynamic activity of the beating heart.

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A computerized device for long-term measurements of the contraction frequency of cultured rat heart cells under stable incubating conditions

Cited by 14 publications

References 18 publications

TGF-β ₁ (Transforming Growth Factor-β ₁ ) Plays a Pivotal Role in Cardiac Myofibroblast Arrhythmogenicity

TGF-β ₁ (Transforming Growth Factor-β ₁ ) Plays a Pivotal Role in Cardiac Myofibroblast Arrhythmogenicity

Power-Law Behavior of Beat-Rate Variability in Monolayer Cultures of Neonatal Rat Ventricular Myocytes

Rigidity Matching between Cells and the Extracellular Matrix Leads to the Stabilization of Cardiac Conduction

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A computerized device for long-term measurements of the contraction frequency of cultured rat heart cells under stable incubating conditions

Cited by 14 publications

References 18 publications

TGF-β 1 (Transforming Growth Factor-β 1 ) Plays a Pivotal Role in Cardiac Myofibroblast Arrhythmogenicity

TGF-β 1 (Transforming Growth Factor-β 1 ) Plays a Pivotal Role in Cardiac Myofibroblast Arrhythmogenicity

Power-Law Behavior of Beat-Rate Variability in Monolayer Cultures of Neonatal Rat Ventricular Myocytes

Rigidity Matching between Cells and the Extracellular Matrix Leads to the Stabilization of Cardiac Conduction

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TGF-β ₁ (Transforming Growth Factor-β ₁ ) Plays a Pivotal Role in Cardiac Myofibroblast Arrhythmogenicity

TGF-β ₁ (Transforming Growth Factor-β ₁ ) Plays a Pivotal Role in Cardiac Myofibroblast Arrhythmogenicity