Relevant bibliographies by topics / Human atrial cardiomyocyte

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  1. Journal articles
  2. Dissertations / Theses
  3. Conference papers

Academic literature on the topic 'Human atrial cardiomyocyte'

Author: Grafiati
Published: 7 September 2024

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Journal articles on the topic "Human atrial cardiomyocyte"

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Schmid, Christina, Najah Abi-Gerges, Michael Leitner, Dietmar Zellner, and Georg Rast. "Ion Channel Expression and Electrophysiology of Singular Human (Primary and Induced Pluripotent Stem Cell-Derived) Cardiomyocytes." Cells 10, no. 12 (November 30, 2021): 3370. http://dx.doi.org/10.3390/cells10123370.

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Subtype-specific human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are promising tools, e.g., to assess the potential of drugs to cause chronotropic effects (nodal hiPSC-CMs), atrial fibrillation (atrial hiPSC-CMs), or ventricular arrhythmias (ventricular hiPSC-CMs). We used single-cell patch-clamp reverse transcriptase-quantitative polymerase chain reaction to clarify the composition of the iCell cardiomyocyte population (Fujifilm Cellular Dynamics, Madison, WI, USA) and to compare it with atrial and ventricular Pluricytes (Ncardia, Charleroi, Belgium) and primary human atrial and ventricular cardiomyocytes. The comparison of beating and non-beating iCell cardiomyocytes did not support the presence of true nodal, atrial, and ventricular cells in this hiPSC-CM population. The comparison of atrial and ventricular Pluricytes with primary human cardiomyocytes showed trends, indicating the potential to derive more subtype-specific hiPSC-CM models using appropriate differentiation protocols. Nevertheless, the single-cell phenotypes of the majority of the hiPSC-CMs showed a combination of attributes which may be interpreted as a mixture of traits of adult cardiomyocyte subtypes: (i) nodal: spontaneous action potentials and high HCN4 expression and (ii) non-nodal: prominent INa-driven fast inward current and high expression of SCN5A. This may hamper the interpretation of the drug effects on parameters depending on a combination of ionic currents, such as beat rate. However, the proven expression of specific ion channels supports the evaluation of the drug effects on ionic currents in a more realistic cardiomyocyte environment than in recombinant non-cardiomyocyte systems.
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Xie, Duanyang, Ke Xiong, Xuling Su, Guanghua Wang, Qiang Ji, Qicheng Zou, Lingling Wang, et al. "Identification of an endogenous glutamatergic transmitter system controlling excitability and conductivity of atrial cardiomyocytes." Cell Research 31, no. 9 (April 6, 2021): 951–64. http://dx.doi.org/10.1038/s41422-021-00499-5.

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AbstractAs an excitatory transmitter system, the glutamatergic transmitter system controls excitability and conductivity of neurons. Since both cardiomyocytes and neurons are excitable cells, we hypothesized that cardiomyocytes may also be regulated by a similar system. Here, we have demonstrated that atrial cardiomyocytes have an intrinsic glutamatergic transmitter system, which regulates the generation and propagation of action potentials. First, there are abundant vesicles containing glutamate beneath the plasma membrane of rat atrial cardiomyocytes. Second, rat atrial cardiomyocytes express key elements of the glutamatergic transmitter system, such as the glutamate metabolic enzyme, ionotropic glutamate receptors (iGluRs), and glutamate transporters. Third, iGluR agonists evoke iGluR-gated currents and decrease the threshold of electrical excitability in rat atrial cardiomyocytes. Fourth, iGluR antagonists strikingly attenuate the conduction velocity of electrical impulses in rat atrial myocardium both in vitro and in vivo. Knockdown of GRIA3 or GRIN1, two highly expressed iGluR subtypes in atria, drastically decreased the excitatory firing rate and slowed down the electrical conduction velocity in cultured human induced pluripotent stem cell (iPSC)-derived atrial cardiomyocyte monolayers. Finally, iGluR antagonists effectively prevent and terminate atrial fibrillation in a rat isolated heart model. In addition, the key elements of the glutamatergic transmitter system are also present and show electrophysiological functions in human atrial cardiomyocytes. In conclusion, our data reveal an intrinsic glutamatergic transmitter system directly modulating excitability and conductivity of atrial cardiomyocytes through controlling iGluR-gated currents. Manipulation of this system may open potential new avenues for therapeutic intervention of cardiac arrhythmias.
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Freundt, Johanna K., Gerrit Frommeyer, Fabian Wötzel, Andreas Huge, Andreas Hoffmeier, Sven Martens, Lars Eckardt, and Philipp S. Lange. "The Transcription Factor ATF4 Promotes Expression of Cell Stress Genes and Cardiomyocyte Death in a Cellular Model of Atrial Fibrillation." BioMed Research International 2018 (May 29, 2018): 1–15. http://dx.doi.org/10.1155/2018/3694362.

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Introduction. Cardiomyocyte remodelling in atrial fibrillation (AF) has been associated with both oxidative stress and endoplasmic reticulum (ER) stress and is accompanied by a complex transcriptional regulation. Here, we investigated the role the oxidative stress and ER stress responsive bZIP transcription factor ATF4 plays in atrial cardiomyocyte viability and AF induced gene expression. Methods. HL-1 cardiomyocytes were subjected to rapid field stimulation. Forced expression of ATF4 was achieved by adenoviral gene transfer. Using global gene expression analysis and chromatin immunoprecipitation, ATF4 dependent transcriptional regulation was studied, and tissue specimen of AF patients was analysed by immunohistochemistry. Results. Oxidative stress and ER stress caused a significant reduction in cardiomyocyte viability and were associated with an induction of ATF4. Accordingly, ATF4 was also induced by rapid field stimulation mimicking AF. Forced expression of wild type ATF4 promoted cardiomyocyte death. ATF4 was demonstrated to bind to the promoters of several cell stress genes and to induce the expression of a number of ATF4 dependent stress responsive genes. Moreover, immunohistochemical analyses showed that ATF4 is expressed in the nuclei of cardiomyocytes of tissue specimen obtained from AF patients. Conclusion. ATF4 is expressed in human atrial cardiomyocytes and is induced in response to different types of cell stress. High rate electrical field stimulation seems to result in ATF4 induction, and forced expression of ATF4 reduces cardiomyocyte viability.
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Nesterova, Tatyana, Dmitry Shmarko, Konstantin Ushenin, and Olga Solovyova. "In-silico analysis of aging mechanisms of action potential remodeling in human atrial cardiomyocites." BIO Web of Conferences 22 (2020): 01025. http://dx.doi.org/10.1051/bioconf/20202201025.

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Electrophysiology of cardiomyocytes changes with aging. Agerelated ionic remodeling in cardiomyocytes may increase the incidence and prevalence of atrial fibrillation (AF) in the elderly and affect the efficiency of antiarrhythmic drugs. There is the deep lack of experimental data on an action potential and transmembrane currents recorded in the healthy human cardiomyocytes of different age. Experimental data in mammals is also incomplete and often contradicting depending on the experimental conditions. In this in-silico study, we used a population of ionic models of human atrial cardiomyocytes to transfer data on the age- related ionic remodeling in atrial cardiomyocytes from canines and mice to predict possible consequences for human cardiomyocyte activity. Based on experimental data, we analyzes two hypotheses on the aging effect on the ionic currents using two age-related sets of varied model parameters and evaluated corresponding changes in action potential morphology with aging. Using the two populations of aging models, we analyzed the agedependent sensitivity of atrial cardiomyocytes to Dofetilide which is one of the antiarrhythmic drugs widely used in patients with atrial fibrillation.
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Li, Jiuru, Alexandra Wiesinger, Lianne Fokkert, Bastiaan J. Boukens, Arie O. Verkerk, Vincent M. Christoffels, Gerard J. J. Boink, and Harsha D. Devalla. "Molecular and electrophysiological evaluation of human cardiomyocyte subtypes to facilitate generation of composite cardiac models." Journal of Tissue Engineering 13 (January 2022): 204173142211279. http://dx.doi.org/10.1177/20417314221127908.

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Paucity of physiologically relevant cardiac models has limited the widespread application of human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes in drug development. Here, we performed comprehensive characterization of hiPSC-derived cardiomyocyte subtypes from 2D and 3D cultures and established a novel 3D model to study impulse initiation and propagation. Directed differentiation approaches were used to generate sinoatrial nodal (SANCM), atrial (ACM) and ventricular cardiomyocytes (VCM). Single cell RNA sequencing established that the protocols yield distinct cell populations in line with expected identities, which was also confirmed by electrophysiological characterization. In 3D EHT cultures of all subtypes, we observed prominent expression of stretch-responsive genes such as NPPA. Response to rate modulating drugs noradrenaline, carbachol and ivabradine were comparable in single cells and EHTs. Differences in the speed of impulse propagation between the subtypes were more pronounced in EHTs compared with 2D monolayers owing to a progressive increase in conduction velocities in atrial and ventricular cardiomyocytes, in line with a more mature phenotype. In a novel binary EHT model of pacemaker-atrial interface, the SANCM end of the tissue consistently paced the EHTs under baseline conditions, which was inhibited by ivabradine. Taken together, our data provide comprehensive insights into molecular and electrophysiological properties of hiPSC-derived cardiomyocyte subtypes, facilitating the creation of next generation composite cardiac models for drug discovery, disease modeling and cell-based regenerative therapies.
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Rajala, Kristiina, Mari Pekkanen-Mattila, and Katriina Aalto-Setälä. "Cardiac Differentiation of Pluripotent Stem Cells." Stem Cells International 2011 (2011): 1–12. http://dx.doi.org/10.4061/2011/383709.

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The ability of human pluripotent stem cells to differentiate towards the cardiac lineage has attracted significant interest, initially with a strong focus on regenerative medicine. The ultimate goal to repair the heart by cardiomyocyte replacement has, however, proven challenging. Human cardiac differentiation has been difficult to control, but methods are improving, and the process, to a certain extent, can be manipulated and directed. The stem cell-derived cardiomyocytes described to date exhibit rather immature functional and structural characteristics compared to adult cardiomyocytes. Thus, a future challenge will be to develop strategies to reach a higher degree of cardiomyocyte maturationin vitro, to isolate cardiomyocytes from the heterogeneous pool of differentiating cells, as well as to guide the differentiation into the desired subtype, that is, ventricular, atrial, and pacemaker cells. In this paper, we will discuss the strategies for the generation of cardiomyocytes from pluripotent stem cells and their characteristics, as well as highlight some applications for the cells.
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Wells, Simon P., Helen M. Waddell, Choon Boon Sim, Shiang Y. Lim, Gabriel B. Bernasochi, Davor Pavlovic, Paulus Kirchhof, Enzo R. Porrello, Lea M. D. Delbridge, and James R. Bell. "Cardiomyocyte functional screening: interrogating comparative electrophysiology of high-throughput model cell systems." American Journal of Physiology-Cell Physiology 317, no. 6 (December 1, 2019): C1256—C1267. http://dx.doi.org/10.1152/ajpcell.00306.2019.

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Cardiac arrhythmias of both atrial and ventricular origin are an important feature of cardiovascular disease. Novel antiarrhythmic therapies are required to overcome current drug limitations related to effectiveness and pro-arrhythmia risk in some contexts. Cardiomyocyte culture models provide a high-throughput platform for screening antiarrhythmic compounds, but comparative information about electrophysiological properties of commonly used types of cardiomyocyte preparations is lacking. Standardization of cultured cardiomyocyte microelectrode array (MEA) experimentation is required for its application as a high-throughput platform for antiarrhythmic drug development. The aim of this study was to directly compare the electrophysiological properties and responses to isoproterenol of three commonly used cardiac cultures. Neonatal rat ventricular myocytes (NRVMs), immortalized atrial HL-1 cells, and custom-generated human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were cultured on microelectrode arrays for 48–120 h. Extracellular field potentials were recorded, and conduction velocity was mapped in the presence/absence of the β-adrenoceptor agonist isoproterenol (1 µM). Field potential amplitude and conduction velocity were greatest in NRVMs and did not differ in cardiomyocytes isolated from male/female hearts. Both NRVMs and hiPSC-CMs exhibited longer field potential durations with rate dependence and were responsive to isoproterenol. In contrast, HL-1 cells exhibited slower conduction and shorter field potential durations and did not respond to 1 µM isoproterenol. This is the first study to compare the intrinsic electrophysiologic properties of cultured cardiomyocyte preparations commonly used for in vitro electrophysiology assessment. These findings offer important comparative data to inform methodological approaches in the use of MEA and other techniques relating to cardiomyocyte functional screening investigations of particular relevance to arrhythmogenesis.
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Hochman-Mendez, Camila, Dilza Balteiro Pereira de Campos, Rafael Serafim Pinto, Bernardo Jorge da Silva Mendes, Gustavo Miranda Rocha, Gustavo Monnerat, Gilberto Weissmuller, et al. "Tissue-engineered human embryonic stem cell-containing cardiac patches: evaluating recellularization of decellularized matrix." Journal of Tissue Engineering 11 (January 2020): 204173142092148. http://dx.doi.org/10.1177/2041731420921482.

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Decellularized cardiac extracellular matrix scaffolds with preserved composition and architecture can be used in tissue engineering to reproduce the complex cardiac extracellular matrix. However, evaluating the extent of cardiomyocyte repopulation of decellularized cardiac extracellular matrix scaffolds after recellularization attempts is challenging. Here, we describe a unique combination of biochemical, biomechanical, histological, and physiological parameters for quantifying recellularization efficiency of tissue-engineered cardiac patches compared with native cardiac tissue. Human embryonic stem cell-derived cardiomyocytes were seeded into rat heart atrial and ventricular decellularized cardiac extracellular matrix patches. Confocal and atomic force microscopy showed cell integration within the extracellular matrix basement membrane that was accompanied by restoration of native cardiac tissue passive mechanical properties. Multi-electrode array and immunostaining (connexin 43) were used to determine synchronous field potentials with electrical coupling. Myoglobin content (~60%) and sarcomere length measurement (>45% vs 2D culture) were used to evaluate cardiomyocyte maturation of integrated cells. The combination of these techniques allowed us to demonstrate that as cellularization efficiency improves, cardiomyocytes mature and synchronize electrical activity, and tissue mechanical/biochemical properties improve toward those of native tissue.
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Dobrev, Dobromir, and Ursula Ravens. "Remodeling of cardiomyocyte ion channels in human atrial fibrillation." Basic Research in Cardiology 98, no. 3 (May 2003): 137–48. http://dx.doi.org/10.1007/s00395-003-0409-8.

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Baena-Montes, Jara M., Tony O’Halloran, Cormac Clarke, Kevin Donaghey, Eoghan Dunne, Martin O’Halloran, and Leo R. Quinlan. "Electroporation Parameters for Human Cardiomyocyte Ablation In Vitro." Journal of Cardiovascular Development and Disease 9, no. 8 (July 28, 2022): 240. http://dx.doi.org/10.3390/jcdd9080240.

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Cardiac ablation with irreversible electroporation (IRE) is quickly being established as a modality of choice for atrial fibrillation treatment. While it has not yet been optimised, IRE has the potential to significantly limit collateral damage and improve cell-specific targeting associated with other energy sources. However, more tissue and cell-specific evidence is required to demonstrate the selective threshold parameters for human cells. The aim here is to determine the optimal ablation threshold parameters related to lesion size for human cardiomyocytes in 2D culture. Conventional biphasic pulses of different field strengths and on-times were delivered in a monolayer culture system of human AC16 cardiomyocytes. The dynamics of cell death and lesion dimensions were examined at different time points. Human cardiomyocytes are susceptible to significant electroporation and cell death at a field strength of 750 V/cm or higher with 100 μs pulses. Increasing the IRE on-time from 3 ms to 60 ms reduces the effective field threshold to 250 V/cm. Using very short pulses of 2 μs and 5 μs also causes significant cell death, but only at fields higher than 1000 V/cm. A longer on-time results in more cell death and induced greater lesion area in 2D models. In addition, different forms of cell death are predicted based on the evolution of cell death over time. This study presents important findings on the ability of different IRE parameters to induce human cardiomyocyte cell death. Lesion size can be tuned by appropriate choice of IRE parameters and cardiomyocytes display an upregulation of delayed cell death 24 h after electroporation, which is an important consideration for clinical practice.
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Dissertations / Theses on the topic "Human atrial cardiomyocyte"

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Boileve, Arthur. "Ιmplicatiοn des prοtéines EΡAC dans la régulatiοn de l'activité électrique des cardiοmyοcytes." Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMC404.

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Les Protéines d’Échange directement Activées par l’AMPc (EPAC) sont des effecteurs majeurs de la voie de l’AMPc. Dans le cardiomyocyte, les protéines EPAC interviennent dans la régulation de nombreuses fonctions cellulaires. Elles participent à la mise en place de processus hypertrophiques et à la régulation de l’homéostasie calcique en contribuant aux mécanismes de fuite de Ca2+ diastolique. Par ailleurs, les protéines EPAC concourent à moduler l’électrophysiologie cardiaque et la question de leur potentiel arythmogène a déjà été soulevée. Néanmoins, leur rôle exact dans la régulation de l’électrophysiologie du cardiomyocyte demeure flou. Dans le cardiomyocyte ventriculaire, l’activation pharmacologique aiguë d’EPAC allonge la durée du Potentiel d’Action (PA) en inhibant des courants K+ repolarisants. La signalisation aboutissant à cet effet était toutefois indéterminée. A l’étage atrial, bien qu’une implication d’EPAC1 était suggérée dans la survenue de fibrillation atriale (FA), les effets d’EPAC sur l’électrophysiologie du cardiomyocyte atrial restaient inconnus.Ce travail a pu déterminer que les deux isoformes d’EPAC et différentes voies de signalisation, incluant une voie PLC-PKC et une voie NOS-PKG, transduisaient l’effet d’EPAC et aboutissaient à l’inhibition des courants K+ à l’origine de l’allongement de la durée du PA dans le cardiomyocyte ventriculaire. A l’étage atrial, nous avons pu confirmer dans un modèle murin et dans des cardiomyocytes atriaux humains isolés que l’activation d’EPAC allongeait la durée du PA par l’inhibition des courants K+. Dans le cardiomyocyte atrial humain, cet effet était transduit par plusieurs voies de signalisation impliquant la CaMKII d’une part et un axe AMPK-NOS-PKG d’autre part. Par ailleurs, nos résultats montrent qu’EPAC1, l’isoforme majoritaire dans le cœur, est surexprimée dans des fragments auriculaires de patients en FA et semble impliquée dans la survenue d’épisode de fibrillation chez la souris. Finalement, un nouvel inhibiteur non-compétitif d’EPAC1, l’AM-001, corrigeait l’altération des courants K+ dépendante d’EPAC dans les cardiomyocytes humains issus de patients en FA mais pas dans les cellules provenant de patients en rythme sinusal.Dans son ensemble, ce travail identifie les protéines EPAC comme des modulateurs de l’électrophysiologie du cardiomyocyte. De plus, il suggère l’implication d’EPAC1 dans les mécanismes d’initiation de la FA
Exchange Proteins directly Activated by cAMP (EPAC) act as major effector of cAMP signaling. In cardiomyocyte, EPAC proteins are able to modulate numerous cellular functions. They contribute to hypertrophic processes and Ca2+ handling regulation by the upregulation of diastolic Ca2+ leak mechanisms. Moreover, EPAC proteins are involved in cardiac electrophysiological modulation and their arrhythmogenic potential has already been proposed. However, their exact implication in the cardiomyocyte electrophysiological modulations remains unclear. In ventricular myocyte, acute pharmacological EPAC activation lengthens the Action Potential (AP) by downregulation of K+ repolarizing currents. Nevertheless, the signaling pathways carrying this effect was unknown. In atria, although EPAC1 involvement was suggested in Atrial Fibrillation (AF) occurrence, the impact of EPAC in electrophysiology at the cellular level remained to be determined.This work has identified that both EPAC isoforms and several signaling axis, including a PLC-PKC pathway and a NOS-PKG pathway, contribute to the EPAC-dependent inhibition of K+ current and consecutive AP lengthening in ventricular cardiomyocyte. In atria, we confirmed in murine model and isolated human atrial cardiomyocyte that EPAC activation lengthens AP by K+ currents downregulation. In human atrial cardiomyocyte, this effect was transduced by different signaling pathways involving CaMKII for one part and an AMPK-NOS-PKG axis for another part. Moreover, our results show that EPAC1, the predominant isoform in the heart, is overexpressed in right auricular appendages from AF patients and seems to be involved in AF occurrence in mouse model. Finally, the new EPAC1 selective non-competitive inhibitor AM-001 corrected the EPAC-induced K+ current alteration in human atrial myocytes from AF patients but not in cells from sinus rhythm patients.Overall, this work characterizes EPAC proteins as modulators of cardiomyocyte electrophysiology. Moreover, our results suggest that EPAC1 is involved in the AF initiation processes
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Jambi, Majed. "Differentiation of Human Atrial Myocytes from Endothelial Progenitor Cell-Derived Induced Pluripotent Stem Cells." Thèse, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31158.

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Recent advances in cellular reprogramming have enabled the generation of embryoniclike cells from virtually any cell of the body. These inducible pluripotent stem cells (iPSCs) are capable of indefinite self-renewal while maintaining the ability to differentiate into all cell types. Nowhere will this technology have a greater impact than in the ability to generate disease and patient-specific cell lines. Here we explore the capacity of human iPSCs reprogrammed from peripheral blood endothelial progenitor cells lines to differentiate into atrial myocytes for the study of patient specific atrial physiology. Methods and Results: Late outgrowth endothelial progenitor cells (EPCs) cultured from clinical blood samples provided a robust cell source for genetic reprogramming. Transcriptome analysis hinted that EPCs would be comparatively more amenable to pluripotent reprogramming than the traditional dermal fibroblast. After 6 passages, EPCs were transduced with a doxycycline inducible lentivirus system encoding human transcription factors OCT4, SOX2, KLF4 and Nanog to permit differentiation after removal of doxycycline. The high endogenous expression of key pluripotency transcripts enhanced the ease of iPSC generation as demonstrated by the rapid emergence of typical iPSC colonies. Following removal of doxycycline, genetically reprogrammed EPC-iPSC colonies displayed phenotypic characteristics identical to human embryonic stem cells and expressed high levels of the pluripotent markers SSEA-4, TRA1-60 and TRA1-81. After exposure to conditions known to favor atrial identity, EPC- iPSC differentiating into sheets of beating cardiomyocytes that expressed high levels of several atrial-specific expressed genes (CACNA1H, KCNA5, and MYL4). Conclusions: EPCs provide a stable platform for genetic reprogramming into a pluripotent state using a doxycycline conditional expression system that avoids reexpression of oncogenic/pluripotent factors. Human EPC-derived iPSC can be differentiated into functional cardiomyocytes that express characteristic markers of atrial identity.
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Wullimann, David. "Discovery of candidate biomarkers for purification of atrial and ventricular cardiomyocytes derived from human pluripotent stemcells : Version 2." Thesis, Högskolan i Skövde, Institutionen för hälsa och lärande, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-16903.

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Ahmad, Faizzan Syed. "A novel human stem cell platform for probing adrenoceptor signaling in iPSC derived cardiomyocytes including those with an adult atrial phenotype." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:17972018-6750-4e5c-8cc9-42e9c381f531.

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Scientific research is propelled by two objectives: Understanding and recognizing the essential biology of life, and deciphering this to uncover possible therapeutics in order to improve quality of life as well as relieve pain from disease. The aim of the work described in this thesis was to dissect the fundamental requirements of induced pluripotent stem cells both in pluripotency and differentiation with a particular focus on atrial specificity. Drug targeting of atrial-specific ion channels has been difficult because of lack of availability of appropriate cardiac cells, and preclinical testing studies have been carried out in non-cardiac cell lines, heterogeneous cardiac populations or animal models that have been unable to accurately represent human cardiomyocyte physiology. Therefore, we sought out to develop a preparation of cardiomyocytes showing an atrial phenotype with adult characteristics from human induced-pluripotent stem cells. A culture programme involving the use of Gremlin 2 allowed differentiation of cardiomyocytes with an atrial phenotype from human induced-pluripotent stem cells. When these differentiated cultures were dissociated into single myocytes a substantial fraction of cells showed a rod-shaped morphology with a single central nucleus that was broadly similar to that observed in cells isolated from atrial chambers of the heart. Immunolabelling of these myocytes for cardiac proteins (including RyR2 receptors, actinin-2, F-actin) showed striations with a sarcomere spacing of slightly less than 2um. The isolated rod-shaped cells were electrically quiescent unless stimulated to fire action potentials with an amplitude of 100 mV from a resting potential of approximately -70 mV. Proteins expressed included those for IK1, IKur channels. Ca2+ Transients recorded from spontaneously beating cultures showed increases in amplitude in response to stimulation of adrenoceptors (both alpha and beta). With the aim of identifying key signaling mechanisms in directing cell fate, our new protocol allowed differentiation of human myocytes with an atrial phenotype and adult characteristics that show functional adrenoceptor signaling pathways and are suitable for investigation of drug effects.
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Conference papers on the topic "Human atrial cardiomyocyte"

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Nesterova, T., D. Shmarko, K. Ushenin, and O. Solovyova. "Age-dependent effects of chronic atrial fibrillation remodeling in population of human atrial cardiomyocyte models." In THE VII INTERNATIONAL YOUNG RESEARCHERS’ CONFERENCE – PHYSICS, TECHNOLOGY, INNOVATIONS (PTI-2020). AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0033019.

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Mazhar, "Fazeelat, Francesco Regazzoni, Chiara Bartolucci, Cristiana Corsi, Luca Dede, Alfio Quarteroni, and Stefano Severi." "A Novel Human Atrial Electromechanical Cardiomyocyte Model with Mechano-Calcium Feedback Effect." In 2022 Computing in Cardiology Conference. Computing in Cardiology, 2022. http://dx.doi.org/10.22489/cinc.2022.195.

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Mazhar, Fazeelat, Chiara Bartolucci, Cristiana Corsi, and Stefano Severi. "Investigation of Key Cellular Targets in Atrial Fibrillation Induced Electromechanical Remodeling Using Human Atrial Cardiomyocytes Model." In 2023 Computing in Cardiology Conference. Computing in Cardiology, 2023. http://dx.doi.org/10.22489/cinc.2023.330.

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Joseph, Jermiah J., Christopher W. McIntyre, and Sanjay R. Kharche. "Proarrhythmic Effects of Electrolyte Imbalance in Virtual Human Atrial and Ventricular Cardiomyocytes*." In 2020 42nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) in conjunction with the 43rd Annual Conference of the Canadian Medical and Biological Engineering Society. IEEE, 2020. http://dx.doi.org/10.1109/embc44109.2020.9176060.

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Mazhar, Fazeelat, Francesco Regazzoni, Chiara Bartolucci, Cristiana Corsi, Luca Dede, Alfio Quarteroni, and Stefano Severi. "Electro-Mechanical Coupling in Human Atrial Cardiomyocytes: Model Development and Analysis of Inotropic Interventions." In 2021 Computing in Cardiology (CinC). IEEE, 2021. http://dx.doi.org/10.23919/cinc53138.2021.9662766.

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Nesterova, T., K. Ushenin, and O. Solovyova. "Effect of dofetilide on electrophysiological function of human atrial cardiomyocytes in different age groups." In ACTUAL PROBLEMS OF ORGANIC CHEMISTRY AND BIOTECHNOLOGY (OCBT2020): Proceedings of the International Scientific Conference. AIP Publishing, 2022. http://dx.doi.org/10.1063/5.0069260.

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Seemann, Gunnar, Axel Loewe, and Eike M. W�lfers. "Effects of Fibroblasts coupling on the Electrophysiology of Cardiomyocytes from Different Regions of the Human Atrium: a Simulation Study." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.380-451.

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