Relevant bibliographies by topics / Cardiomyocytes

Academic literature on the topic 'Cardiomyocytes'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 September 2024

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Journal articles on the topic "Cardiomyocytes"

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Nguyen, Phong D., Sarah T. Hsiao, Priyadharshini Sivakumaran, Shiang Y. Lim, and Rodney J. Dilley. "Enrichment of neonatal rat cardiomyocytes in primary culture facilitates long-term maintenance of contractility in vitro." American Journal of Physiology-Cell Physiology 303, no. 12 (December 15, 2012): C1220—C1228. http://dx.doi.org/10.1152/ajpcell.00449.2011.

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Long-term culture of primary neonatal rat cardiomyocytes is limited by the loss of spontaneous contractile phenotype within weeks in culture. This may be due to loss of contractile cardiomyocytes from the culture or overgrowth of the non-cardiomyocyte population. Using the mitochondria specific fluorescent dye, tetramethylrhodamine methyl ester perchlorate (TMRM), we showed that neonatal rat cardiomyocytes enriched by fluorescence-activated cell sorting can be maintained as contractile cultures for long periods (24-wk culture vs. 2 wk for unsorted cardiomyocytes). Long-term culture of this purified cardiomyocyte (TMRM high) population retained the expression of cardiomyocyte markers, continued calcium cycling, and displayed cyclic electrical activity that could be regulated pharmacologically. These findings suggest that non-cardiomyocyte populations can negatively influence contractility of cardiomyocytes in culture and that by purifying cardiomyocytes, the cultures retain potential as an experimental model for longitudinal studies of cardiomyocyte biology in vitro.
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Derks, Wouter, and Olaf Bergmann. "Polyploidy in Cardiomyocytes." Circulation Research 126, no. 4 (February 14, 2020): 552–65. http://dx.doi.org/10.1161/circresaha.119.315408.

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The hallmark of most cardiac diseases is the progressive loss of cardiomyocytes. In the perinatal period, cardiomyocytes still proliferate, and the heart shows the capacity to regenerate upon injury. In the adult heart, however, the actual rate of cardiomyocyte renewal is too low to efficiently counteract substantial cell loss caused by cardiac injury. In mammals, cardiac growth by cell number expansion changes to growth by cardiomyocyte enlargement soon after birth, coinciding with a period in which most cardiomyocytes increase their DNA content by multinucleation and nuclear polyploidization. Although cardiomyocyte hypertrophy is often associated with these processes, whether polyploidy is a prerequisite or a consequence of hypertrophic growth is unclear. Both the benefits of cardiomyocyte enlargement over proliferative growth of the heart and the physiological role of polyploidy in cardiomyocytes are enigmatic. Interestingly, hearts in animal species with substantial cardiac regenerative capacity dominantly comprise diploid cardiomyocytes, raising the hypothesis that cardiomyocyte polyploidy poses a barrier for cardiomyocyte proliferation and subsequent heart regeneration. On the contrary, there is also evidence for self-duplication of multinucleated myocytes, suggesting a more complex picture of polyploidy in heart regeneration. Polyploidy is not restricted to the heart but also occurs in other cell types in the body. In this review, we explore the biological relevance of polyploidy in different species and tissues to acquire insight into its specific role in cardiomyocytes. Furthermore, we speculate about the physiological role of polyploidy in cardiomyocytes and how this might relate to renewal and regeneration.
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Zhang, Yidi, Xin Zhao, and Yaowei Liu. "A visual detection method of cardiomyocyte relaxation and contraction." AIP Advances 13, no. 2 (February 1, 2023): 025028. http://dx.doi.org/10.1063/5.0133456.

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Contraction and relaxation are important functions of cardiomyocytes, and measuring their characteristics provides an evaluation index to explore the effects of drugs on cardiomyocytes. In addition, cardiomyocytes have an innate advantage in acting as a biopower by virtue of their ability to contract and relax, which also requires the detection of cardiomyocyte actions. However, existing measurement methods, such as mechanosensor measurements and calcium concentration measurements, have high requirements for experimental equipment and operation and are challenging to perform simultaneously with other cellular manipulations. Here, we propose a simple visual detection method for cardiomyocyte contraction and relaxation. We first recorded the contraction and relaxation of cardiomyocytes under a bright-field microscope, then used the optical flow method to track the sampling points on the cardiomyocytes in the video, and obtained the frequency of cardiomyocyte contraction and relaxation by analyzing the optical flow matrices. This method does not require the use of additional equipment or additional processing of cardiomyocytes, which significantly reduces the operational difficulty of detection and provides a method to achieve real-time detection of cardiomyocyte contraction and relaxation.
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Lieben Louis, Xavier, Pema Raj, Zach Meikle, Liping Yu, Shannel E. Susser, Shayla MacInnis, Todd A. Duhamel, Jeffrey T. Wigle, and Thomas Netticadan. "Resveratrol prevents palmitic-acid-induced cardiomyocyte contractile impairment." Canadian Journal of Physiology and Pharmacology 97, no. 12 (December 2019): 1132–40. http://dx.doi.org/10.1139/cjpp-2019-0051.

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Long-chain saturated fatty acids, especially palmitic acid (PA), contribute to cardiomyocyte lipotoxicity. This study tests the effects of PA on adult rat cardiomyocyte contractile function and proteins associated with calcium regulating cardiomyocyte contraction and relaxation. Adult rat cardiomyocytes were pretreated with resveratrol (Resv) and then treated with PA. For the reversal study, cardiomyocytes were incubated with PA prior to treatment with Resv. Cardiomyocyte contractility, ratio of rod- to round-shaped cardiomyocytes, and Hoechst staining were used to measure functional and morphological changes in cardiomyocytes. Protein expression of sarco-endoplasmic reticulum ATPase 2a (SERCA2a), native phospholamban (PLB) and phosphorylated PLB (pPLB ser16 and pPLB thr17), and troponin I (TnI) and phosphorylated TnI (pTnI) were measured. SERCA2a activity was also measured. Our results show that PA (200 μM) decreased the rate of cardiomyocyte relaxation, reduced the number of rod-shaped cardiomyocytes, and increased the number of cells with condensed nuclei; pre-treating cardiomyocytes with Resv significantly prevented these changes. Post-treatment with Resv did not reverse morphological changes induced by PA. Protein expression levels of SERCA2a, PLB, pPLBs, TnI, and pTnI were unchanged by PA or Resv. SERCA2a activity assay showed that Vmax and Iono ratio were increased with PA and pre-treatment with Resv prevented this increase. In conclusion, our results show that Resv protect cardiomyocytes from contractile dysfunction induced by PA.
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Stopp, Sabine, Marco Gründl, Marc Fackler, Jonas Malkmus, Marina Leone, Ronald Naumann, Stefan Frantz, et al. "Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development." Proceedings of the National Academy of Sciences 114, no. 30 (July 11, 2017): 8029–34. http://dx.doi.org/10.1073/pnas.1703406114.

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GAS2L3 is a recently identified cytoskeleton-associated protein that interacts with actin filaments and tubulin. The in vivo function of GAS2L3 in mammals remains unknown. Here, we show that mice deficient in GAS2L3 die shortly after birth because of heart failure. Mammalian cardiomyocytes lose the ability to proliferate shortly after birth, and further increase in cardiac mass is achieved by hypertrophy. The proliferation arrest of cardiomyocytes is accompanied by binucleation through incomplete cytokinesis. We observed that GAS2L3 deficiency leads to inhibition of cardiomyocyte proliferation and to cardiomyocyte hypertrophy during embryonic development. Cardiomyocyte-specific deletion of GAS2L3 confirmed that the phenotype results from the loss of GAS2L3 in cardiomyocytes. Cardiomyocytes fromGas2l3-deficient mice exhibit increased expression of a p53-transcriptional program including the cell cycle inhibitor p21. Furthermore, loss of GAS2L3 results in premature binucleation of cardiomyocytes accompanied by unresolved midbody structures. Together these results suggest that GAS2L3 plays a specific role in cardiomyocyte cytokinesis and proliferation during heart development.
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Mensah, Isaiah K., and Humaira Gowher. "Signaling Pathways Governing Cardiomyocyte Differentiation." Genes 15, no. 6 (June 18, 2024): 798. http://dx.doi.org/10.3390/genes15060798.

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Cardiomyocytes are the largest cell type that make up the heart and confer beating activity to the heart. The proper differentiation of cardiomyocytes relies on the efficient transmission and perception of differentiation cues from several signaling pathways that influence cardiomyocyte-specific gene expression programs. Signaling pathways also mediate intercellular communications to promote proper cardiomyocyte differentiation. We have reviewed the major signaling pathways involved in cardiomyocyte differentiation, including the BMP, Notch, sonic hedgehog, Hippo, and Wnt signaling pathways. Additionally, we highlight the differences between different cardiomyocyte cell lines and the use of these signaling pathways in the differentiation of cardiomyocytes from stem cells. Finally, we conclude by discussing open questions and current gaps in knowledge about the in vitro differentiation of cardiomyocytes and propose new avenues of research to fill those gaps.
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Zhang, Jun, Yuying Gao, Peng Chen, Yu Zhou, Sheng Guo, Li Wang, and Jie Chen. "Bone Marrow-Derived Mesenchymal Stem Cells (BMSCs)-Exosome Carrying MiRNA-312 Inhibits Sevoflurane-Induced Cardiomyocyte Apoptosis Through Activation of Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/AKT) Pathway." Journal of Biomaterials and Tissue Engineering 12, no. 5 (May 1, 2022): 947–52. http://dx.doi.org/10.1166/jbt.2022.2971.

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This study was to explore the mechanism by how exosomes (exo) derived from BMSCs affects cardiomyocyte apoptosis. BMSCs were isolated and incubated with cardiomyocytes while the cardiomyocytes were exposed to sevoflurane or DMSO treatment. Apoptotic cells were calculated and level of apoptosis related proteins was detected by Western blot. Through transfection with microRNA-(miRNA)-312 inhibitor, we evaluated the effect of BMSC-exo on the sevoflurane-induced apoptosis. Sevoflurane significantly inhibited the viability of cardiomyocytes and induced cardiomyocyte apoptosis. Besides, sevoflurane decreased the expression of miR-312 and enhanced Bax expression in cardiomyocytes through restraining the phosphorylation of MAPK/ERK. Treatment with BMSC-exo, however, activated MAPK/ERK signaling by up-regulating miR-312, thereby inhibiting cardiomyocyte apoptosis, promoting cardiomyocyte proliferation, and elevating the level of Bcl-2. In conclusion, BMSC-exo-derived miR-312 inhibits sevoflurane-induced cardiomyocyte apoptosis by activating PI3K/AKT signaling pathway.
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Chiu, Chiung-Zuan, Bao-Wei Wang, Tun-Hui Chung, and Kou-Gi Shyu. "Angiotensin II and the ERK pathway mediate the induction of myocardin by hypoxia in cultured rat neonatal cardiomyocytes." Clinical Science 119, no. 7 (June 22, 2010): 273–82. http://dx.doi.org/10.1042/cs20100084.

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Hypoxic injury to cardiomyocytes is a stress that causes cardiac pathology through cardiac-restricted gene expression. SRF (serum-response factor) and myocardin are important for cardiomyocyte growth and differentiation in response to myocardial injuries. Previous studies have indicated that AngII (angiotensin II) stimulates both myocardin expression and cardiomyocyte hypertrophy. In the present study, we evaluated the expression of myocardin and AngII after hypoxia in regulating gene transcription in neonatal cardiomyocytes. Cultured rat neonatal cardiomyocytes were subjected to hypoxia, and the expression of myocardin and AngII were evaluated. Different signal transduction pathway inhibitors were used to identify the pathway(s) responsible for myocardin expression. An EMSA (electrophoretic mobility-shift assay) was used to identify myocardin/SRF binding, and a luciferase assay was used to identify transcriptional activity of myocardin/SRF in neonatal cardiomyocytes. Both myocardin and AngII expression increased after hypoxia, with AngII appearing at an earlier time point than myocardin. Myocardin expression was stimulated by AngII and ERK (extracellular-signal-regulated kinase) phosphorylation, but was suppressed by an ARB (AngII type 1 receptor blocker), an ERK pathway inhibitor and myocardin siRNA (small interfering RNA). AngII increased both myocardin expression and transcription in neonatal cardiomyocytes. Binding of myocardin/SRF was identified using an EMSA, and a luciferase assay indicated the transcription of myocardin/SRF in neonatal cardiomyocytes. Increased BNP (B-type natriuretic peptide), MHC (myosin heavy chain) and [3H]proline incorporation into cardiomyocytes was identified after hypoxia with the presence of myocardin in hypertrophic cardiomyocytes. In conclusion, hypoxia in cardiomyocytes increased myocardin expression, which is mediated by the induction of AngII and the ERK pathway, to cause cardiomyocyte hypertrophy. Myocardial hypertrophy was identified as an increase in transcriptional activities, elevated hypertrophic and cardiomyocyte phenotype markers, and morphological hypertrophic changes in cardiomyocytes.
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Takaoka, Nanako, Michiko Yamane, Ayami Hasegawa, Koya Obara, Kyoumi Shirai, Ryoichi Aki, Hiroyasu Hatakeyama, et al. "Rat hair-follicle-associated pluripotent (HAP) stem cells can differentiate into atrial or ventricular cardiomyocytes in culture controlled by specific supplementation." PLOS ONE 19, no. 1 (January 26, 2024): e0297443. http://dx.doi.org/10.1371/journal.pone.0297443.

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There has been only limited success to differentiate adult stem cells into cardiomyocyte subtypes. In the present study, we have successfully induced beating atrial and ventricular cardiomyocytes from rat hair-follicle-associated pluripotent (HAP) stem cells, which are adult stem cells located in the bulge area. HAP stem cells differentiated into atrial cardiomyocytes in culture with the combination of isoproterenol, activin A, bone morphogenetic protein 4 (BMP4), basic fibroblast growth factor (bFGF), and cyclosporine A (CSA). HAP stem cells differentiated into ventricular cardiomyocytes in culture with the combination of activin A, BMP4, bFGF, inhibitor of Wnt production-4 (IWP4), and vascular endothelial growth factor (VEGF). Differentiated atrial cardiomyocytes were specifically stained for anti-myosin light chain 2a (MLC2a) antibody. Ventricular cardiomyocytes were specially stained for anti-myosin light chain 2v (MLC2v) antibody. Quantitative Polymerase Chain Reaction (qPCR) showed significant expression of MLC2a in atrial cardiomyocytes and MLC2v in ventricular cardiomyocytes. Both differentiated atrial and ventricular cardiomyocytes showed characteristic waveforms in Ca2+ imaging. Differentiated atrial and ventricular cardiomyocytes formed long myocardial fibers and beat as a functional syncytium, having a structure similar to adult cardiomyocytes. The present results demonstrated that it is possible to induce cardiomyocyte subtypes, atrial and ventricular cardiomyocytes, from HAP stem cells.
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Shi, Huairui, Xuehong Zhang, Zekun He, Zhiyong Wu, Liya Rao, and Yushu Li. "Metabolites of Hypoxic Cardiomyocytes Induce the Migration of Cardiac Fibroblasts." Cellular Physiology and Biochemistry 41, no. 1 (2017): 413–21. http://dx.doi.org/10.1159/000456531.

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Background: The migration of cardiac fibroblasts to the infarct region plays a major role in the repair process after myocardial necrosis or damage. However, few studies investigated whether early hypoxia in cardiomyocytes induces the migration of cardiac fibroblasts. The purpose of this study was to assess the role of metabolites of early hypoxic cardiomyocytes in the induction of cardiac fibroblast migration. Methods: Neonatal rat heart tissue was digested with a mixture of trypsin and collagenase at an appropriate ratio. Cardiomyocytes and cardiac fibroblasts were cultured via differential adhesion. The cardiomyocyte cultures were subjected to hypoxia for 2, 4, 6, 8, 10, and 12 h. The supernatants of the cardiomyocyte cultures were collected to determine the differences in cardiac fibroblast migration induced by hypoxic cardiomyocyte metabolites at various time points using a Transwell apparatus. Meanwhile, ELISA was performed to measure TNF-α, IL-1β and TGF-β expression levels in the cardiomyocyte metabolites at various time points. Results: The metabolites of hypoxic cardiomyocytes significantly induced the migration of cardiac fibroblasts. The induction of cardiac fibroblast migration was significantly enhanced by cardiomyocyte metabolites in comparison to the control after 2, 4, and 6 h of hypoxia, and the effect was most significant after 2 h. The expression levels of TNF-α, IL-1β, IL-6, and TGF-β were substantially increased in the metabolites of cardiomyocytes, and neutralization with anti-TNF-α and anti-IL-1β antibodies markedly reduced the induction of cardiac fibroblast migration by the metabolites of hypoxic cardiomyocytes. Conclusion: The metabolites of early hypoxic cardiomyocytes can induce the migration of cardiac fibroblasts, and TNF-α and IL-1β may act as the initial chemotactic inducers.
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Dissertations / Theses on the topic "Cardiomyocytes"

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Maggiorani, Damien. "Caractérisation de la sénescence des cardiomyocytes et identification de marqueurs associés." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30320/document.

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Le vieillissement de l'organisme prédispose à de nombreuses pathologies chroniques telles que l'insuffisance cardiaque (IC). Des études récentes ont montré que l'accumulation de cellules sénescentes dans les organes au cours du vieillissement est associée à l'apparition de ces pathologies. La sénescence cellulaire a initialement été décrite comme un arrêt stable du cycle cellulaire permettant de limiter la prolifération des cellules dont l'ADN est endommagé. Ce processus s'accompagne de profondes modifications de la fonction cellulaire, avec notamment l'acquisition d'un phénotype sécrétoire associé à la sénescence. La sénescence peut être induite par un raccourcissement des télomères ou par l'exposition à des signaux de stress, tels que le stress oxydant ou l'irradiation, qui entrainent l'activation de la réponse cellulaire aux dommages de l'ADN et l'expression des gènes suppresseurs de tumeurs (p16INK4a, p21CIP1, p53). Ces inhibiteurs du cycle cellulaire sont classiquement utilisés comme marqueur de sénescence car leur expression augmente de manière ubiquitaire au cours du vieillissement. Toutefois, ces marqueurs ne sont pas spécifiques du tissu concerné et un des objectifs de ma thèse a été d'identifier de nouveaux marqueurs de sénescence tissu-spécifiques qui pourraient caractériser un vieillissement cardiaque pathologique. Le vieillissement cardiaque se caractérise par une hypertrophie des cardiomyocytes, une sensibilité accrue au stress et une prédisposition à l'IC. Les cardiomyocytes étant des cellules post-mitotiques, les mécanismes de sénescence mis en jeu, les marqueurs associés et leur rôle potentiel dans l'IC demeurent à l'heure actuelle peu caractérisés. Au cours de ce travail de thèse nous avons donc entrepris : 1) d'étudier le rôle des télomères et des dysfonctions mitochondriales dans l'induction de la sénescence du cardiomyocyte et 2) d'identifier des marqueurs spécifiques. Nous avons tout d'abord montré que les cardiomyocytes de souris âgées expriment les marqueurs classiques de la sénescence comme p16INK4a, p53 et p21CIP1. Concernant les mécanismes inducteurs, nous avons étudié l'implication des dommages télomériques (telomere associated foci, TAF). Au cours du vieillissement, nous avons observé une augmentation du nombre de TAFs par cardiomyocytes en association avec l'hypertrophie. De plus, l'induction de TAFs in vitro est suffisante à l'activation de la voie de sénescence p53/p21CIP1 et l'hypertrophie dans une lignée de cardiomyoblastes H9c2. La formation des TAFs est augmentée chez des souris avec une dysfonction mitochondriale et est associée à l'activation des voies p53/p21CIP1. Par ailleurs, les cardiomyocytes âgés présentent une dérégulation des gènes impliqués dans la biologie mitochondriale pouvant rendre compte de l'augmentation des TAFs. Par l'analyse haut débit du transcriptome (RNAseq) nous avons identifié six nouveaux gènes qui sont surexprimés dans les cardiomyocytes sénescents (Prom2, Kcnk1, Pah, Edn3, Gdf15, Tgfb2). La comparaison d'expression de ces gènes dans le cœur avec d'autres tissus et avec le stroma cardiaque lors vieillissement a permis de confirmer la spécificité d'expression de ces marqueurs au niveau des cardiomyocytes. Nous avons validé cette signature dans deux modèles in vitro de sénescence induite par le stress et démontré que l'expression de certains de ces marqueurs est dépendante de la voie p53. De plus, l'expression de Prom2 est associée à l'hypertrophie des cardiomyocytes. En conclusion, nous avons démontré, qu'avec le vieillissement, les cardiomyocytes présentent un programme de sénescence associé à une dysfonction mitochondriale et une augmentation des TAFs. Cette sénescence se caractérise par l'activation des voies classiques de sénescence (p16INK4, p53/p21CIP1), une hypertrophie et l'acquisition d'une signature spécifique. Ces marqueurs offrent de nouvelles perspectives dans la compréhension de la sénescence cardiaque et dans son implication potentielle dans l'IC
Ageing of the organism is associated with several chronic pathologies such as heart failure (HF). Recent studies have demonstrated the link between the accumulation of senescent cells during ageing and age-associated diseases. Cellular senescence, originally defined as a stable cell cycle arrest, acts as a tumorigenic repressor by limiting the proliferation of DNA damaged cells. Despite this protective effect, senescence is characterized by deep remodeling of cell biology which drives functional disorders, such as the acquisition of a senescence-associated secretory phenotype (SASP). Senescence can be induced by telomeric attrition and by exposition to cellular stress signals such as oxidative stress or irradiation, which induce telomeric damage, activation of the DNA Damage Response (DDR) and increased expression of antitumoral genes (p16INK4a, p21CIP1, p53). These genes are classically used as markers of senescence because their expression increases in several tissues during ageing but they are not tissue-specific. Therefore, At the cardiac level, ageing is characterized by cardiomyocytes hypertrophy, increased sensitivity to stress and highest risk of developing HF. Cardiomyocytes are post- mitotic cells and the senescence inductor mechanisms, specifics markers and their role in HF remains poorly understood. This thesis project is articulated around two aims, 1/ studying the role of telomeric damages and mitochondrial dysfunction in triggering cardiomyocyte senescence and 2/ identification of specifics markers. Fisrtly, we shown that aged cardiomyocytes overexpress classic markers of senescence such as p16INK4a, p53 et p21CIP1. Concerning the inductors mechanisms, we studied the implication of telomeric damages (telomere associated foci, TAF). During ageing, we found an increased number of TAFs per cardiomyocytes and their association with hypertrophy. Moreover, TAF- induction in cardiac H9c2 in vitro activated the p53/p21 pathway and induced senescence. These data confirmed the role of TAFs in cardiomyocyte senescence induction. Furthermore, aged cardiomyocytes exhibit a global alteration of genes involved in mitochondrial biology, oxidative stress and metabolism in aged cardiomyocytes that could play a prominent role in TAF accumulation with ageing. In a second part of the study, by using a next generation sequencing method (RNA-seq) we identified 6 new genes highly expressed in senescent cardiomyocytes (Prom2, Kcnk1, Pah, Edn3, Gdf15 and Tgfb2). Expression comparison with other senescent organs and cardiac stromal cells confirmed these new genes as cardiomyocyte specific. Thanks to an in vitro approach, we validate this signature by using different models of stress-induced senescence in cardiac H9c2 cells and demonstrated the implication of the p53 in the regulation of some of these genes. Moreover, Prom2 expression is associated with cardiomyocytes hypertrophy. In conclusion, we demonstrated that, with ageing, cardiomyocytes display a senescence phenotype associated with mitochondrial dysfunction and TAFs. This process is characterized by classic markers (p16INK4, p53/p21CIP1), hypertrophy and new identified signature. These new markers offer innovative perspectives in the understanding and the identification of the cardiac senescence and their potential deleterious role in heart failure
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Nelson, Brandon John. "MicroRNA analysis of human embryonic stem cell derived cardiomyocytes and neonatal rat ventricular cardiomyocytes." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p1447322.

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Thesis (M.S.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed January 15, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 45-48).
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Bond, Richard. "Cellular electrophysiology of rat pulmonary vein cardiomyocytes : a comparative study with left atrial cardiomyocytes." Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.685358.

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Although atrial fibrillation (AF) is the most common sustained arrhythmia, its pathophysiology is complex and remains poorly understood. Most episodes of AF are initiated by ectopic beats originating from the pulmonary veins (PVs). It has been suggested that the distinct electrophysiological properties of the PVs and their rich innervation by noradrenergic sympathetic fibres contribute to the susceptibility of this region to ectopic activity. This study aimed to determine whether the cellular electrophysiological responses to noradrenaline (NA) of card iomyocytes isolated from the PVs differed to those isolated from the left atrium (LA).
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Fijnvandraat, Arnoldus Cornelis. "Embryonic stem cell-derived cardiomyocytes." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/68354.

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Risto, Morten. "Modelling hypertrophy in dystrophic cardiomyocytes." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3402.

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Duchenne Muscular Dystrophy (DMD) is an X-linked disorder, caused by mutations in the DMD gene. This gene encodes dystrophin, a structural protein that links the sarcomere to the extracellular matrix via a trans-membrane protein complex. In the absence of dystrophin the associated glycoprotein complex fails to assemble, leading to sarcolemmal instability, impaired ion handling, skeletal muscle wasting and fibrosis. Patients become non-ambulant in their teens and seldom live past their third decade. Cardiac failure is one of the leading causes of death. The heart initially compensates for reduced functional capacity by becoming hypertrophic, but eventually becomes fibrotic and develops dilated cardiomyopathy. Several proposed therapies have now reached clinical trial phase, but there is still no cure available for all DMD patients. Some of these therapies target skeletal muscle better than the heart. Sample availability restricts research into cardiac mechanisms of disease and testing treatments. This thesis presents a model that can potentially be used as an in vitro outcome measure for testing DMD therapies. Cardiomyocytes isolated from hearts collected from the DMD mouse model (mdx) embryos became larger than control mouse embryo-derived cardiomyocytes in response to serum starvation in culture. Control and mdx cardiomyocytes were collected at five timepoints of serum starvation and RNA-Seq was performed on the samples to identify pathways responsible for this hypertrophic response observed in dystrophic cells. Several pharmacological compounds as well as a proposed gene therapy method were trialled for their ability to reduce the hypertrophic response. Serum starved cardiomyocytes from mdx mouse embryos were transduced with adeno-associated viruses containing a gene construct expressing a functional internally truncated version of dystrophin. The viral rescue therapy and some pharmacological compounds significantly reduced the dystrophic hypertrophy caused by serum starvation. This model of mdx cardiomyocyte hypertrophy could therefore be used for testing therapies in pre-clinical trials.
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De, Marco Margot. "BAG3 role in cardiomyocytes physiopathology." Doctoral thesis, Universita degli studi di Salerno, 2013. http://hdl.handle.net/10556/896.

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2010 - 2011
The anti-apoptotic protein BAG3 is expressed at high levels in skeletal and cardiac muscle in vivo. Our group recently focused its interest on BAG3 role in myocardiocyte proliferation, survival and response to stressful stimuli. We found that BAG3 is upregulated during the differentiation of cardiomyoblasts. Our results prompted us to verify whether bag3 silencing could affect the differentiation state of cardiocytes and we found that bag3 silencing resulted in highly reducing the levels of myogenin. Furthermore, we analyzed BAG3 expression and localization following cell exposure to oxidative stress. In particular, we found that epinephrine in vitro increases BAG3 expression in adult human cardiomyocytes. We evaluated whether BAG3 could be involved in the Tako-tsubo cardiomyopathy (or stress cardiomyopathy) pathogenesis that is characterized by left ventricular dysfunction, with symptoms that can mimic an acute coronary syndrome. The absence of significant cardiovascular risk factors in patients affected by stress cardiomyopathy suggested that it might be associated with a possible genetic etiology. Therefore, we sequenced bag3 gene to check for polymorphisms in 29 patients and 1043 healthy donors. Three polymorphism were highly represented among patients (R71Q, C151R, P407L). We also showed for the first time that BAG3 protein is released from stressed cardiomyocytes and is found in chronic heart failure (HF) patients’ sera. Since anti-BAG3 antibodies are also present in patients’ sera, we developed an ELISA test for their specific detection. In serum samples from chronic HF patients, we found significantly higher values of anti-BAG3 antibodies respect to samples from healthy donors. The presence of anti-BAG3 antibodies in chronic HF patients’ sera and the availability of an ELISA test for their detection can contribute a novel tool for diagnostic and prognostic evaluations. [edited by author]
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Driesen, Ronald Bertie Mario Antonio. "Adaptive remodeling of cardiomyocytes under stress." [Maastricht] : Maastricht : Universitaire Pers Maastricht ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=11068.

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Kemeny, Naomi. "Alendronate affects calcium dynamics in cardiomyocytes." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40684.

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Alendronate (ALN) is effective in the treatment of osteoporosis. However, ALN has been recently associated with an increased risk of serious atrial fibrillation. We investigated the effects of ALN on cytosolic free calcium concentration ([Ca2+]i) in cardiomyocytes. HL-1 atrial cardiomyocytes were loaded with fura-2 and examined using microspectrofluorimetry. ALN (10-8, 10-7, 10-6 M) induced transitory high frequency oscillations of [Ca2+]i with greater frequency for 10-8 M ALN (61 ± 10 mHz) compared to 10-6 ALN (42 ± 4 mHz). In cells treated with 10-6 M ALN responses to subsequent application of caffeine were delayed, and exhibited a decrease in the rate and amplitude of [Ca2+]i increase. Long term (48 h) exposure to 10-8 M Alendronate resulted in delay of caffeine-induced Ca2+ transients and decreased rate of [Ca2+]i increase, followed by oscillations in [Ca2+]i of 54 ± 8 mHz versus those observed at higher concentrations of Alendronate (35 ± 5 mHz). Changes in calcium dynamics were accompanied by significant changes in the expression of sarcoendoplasmic reticulum ATPase (SERCA2a), calsequestrin and calreticulin.
Alendronate est efficace dans le traitement de l’ostéoporose. Alendronate a récemment été associe avec une risque élevé de fibrillation auriculaire sérieux. On a examine les effets d’Alendronate sur la de calcium cytosolique ([Ca2+]i) dans les cellules musculaires cardiaques. Les cellules musculaires cardiaques HL-1 étaient chargés avec Fura-2 et examinés par microspectrofluorimetrie. Alendronate (10-8, 10-7, 10-6 M) ont provoqués des oscillations de [Ca2+]i fugaces et haute fréquences à 10-8 M Alendronate (61 ± 10 mHz) comparé aux concentrations plus hautes (42 ± 4 mHz). Dans les cellules traits avec 10-6 M ALN, la réponse à l’application de caféine était avec délai, et a manifesté un diminution dans la rythme et amplitude d’augmentation de [Ca2+]i. L’exposition a l’ALN à long terme (48 h) ont provoqué un délai des élévations de calcium transitoires, et un diminution du rythme d’augmentation de [Ca2+]i suites par les oscillations de [Ca2+]i, caractérisés par un augmentation de fréquences avec 10-8 M Alendronate (54 ± 8 mHz) compare aux concentrations plus hautes (35 ± 5 mHz). Le changement des dynamiques de calcium étaient accompagnés par les changements considérables dans l’expression d’ATPase (SERCA2a), calsequestrin et calreticulin du réticulum sarcoendoplasmique.
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9

Bowers, Keith Cyril. "Pathophysiology of ATP in single cardiomyocytes." Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316576.

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Bowman, Peter Ronald Thomas. "Regulation of glucose transport in cardiomyocytes." Thesis, University of Glasgow, 2019. http://theses.gla.ac.uk/41002/.

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Major common complications of diabetes such as myocardial infarction arise from the onset of vascular disease. However, there is also evidence of a direct impairment of cardiac contractile function in diabetic individuals in the absence of atherosclerosis and hypertension, termed diabetic cardiomyopathy (DCM). This is characterised by early diastolic dysfunction that progresses to systolic dysfunction and heart failure through a pathological remodelling process. The earliest identified mechanism underlying this disease is the onset of metabolic perturbations such as cardiac insulin resistance. However, currently there are no specific treatments available, partly due to the lack of an appropriate experimental model with which translational research could be performed. iPSC-CM are a recently developed technology, whereby human dermal fibroblasts can be reliably harvested, dedifferentiated into a pluripotent form, and then differentiated into cardiomyocytes. These cells have an established intracellular calcium handling system and contractile capacity, however are generally considered to be at a foetal stage of development. A key aim of this project was to characterise the metabolic phenotype of these cells, in order to assess their potential suitability as the basis of a novel cellular model of DCM. Specifically, it was investigated if these cells exhibited robust insulin stimulated glucose uptake through insulin sensitive intracellular trafficking of the glucose transporter GLUT4, as impairment of this response is a central feature of any diabetic model. After adaptation of a [3H]-2-deoxyglucose uptake assay to a 96-well plate format, and optimisation of experimental factors, it was determined that iPSC-CM could not display robust insulin (or IGF-1) stimulated glucose uptake. Inhibition of the spontaneous contractile capacity of these cells did not induce a response upon subsequent insulin stimulation. iPSC-CM were found to express and activate central insulin signalling molecules such as Akt and Erk1/2, and also possess elements of the GLUT4 trafficking machinery such as the SNARE proteins Syntaxin 4 and SNAP23. However, the critically limiting factor identified was an approximate 10-fold lower expression of GLUT4 in iPSC-CM compared to primary adult cardiomyocytes, accompanied by strong expression of GLUT1. This data was supported by the finding that inhibition of GLUT4 had no impact on glucose uptake in iPSC-CM, whereas inhibition of GLUT1 significantly reduced uptake by ~50%. This phenotype suggests that iPSC-CM are also at a foetal-like stage of development with regards to their metabolic capacity, and are currently not suitable for modelling DCM. Subsequently, initial interventions based upon the literature were implemented in order to try and increase iPSC-CM GLUT4 content. However, neither increasing metabolic reliance upon fatty acid (rather than glucose) nor exposure to triiodothyronine were successful. In contrast, Lipofectamine 2000 mediated transfection of a customised GLUT4 plasmid facilitated a reliable 3-5 fold increase in iPSC-CM GLUT4 content. This increased basal glucose uptake, however did not induce an insulin response. It was concluded that a further increase in expression levels may be required. Finally, it was demonstrated that iPSC-CM are highly amenable to lentiviral mediated infection, and initial steps were taken towards the generation of a virus targeting the overexpression of GLUT4. Additionally, SNARE proteins are essential in facilitating insulin stimulated GLUT4 expression at the plasma membrane. Therefore they represent a possible mechanism by which cardiac insulin resistance could occur in disease states such as DCM. On account of this, the expression of a wide range of SNARE protein isoforms was assessed in cardiac lysates generated from 2 diabetic mouse models (db/db and high fat diet induced). The expression of SNAP29 and VAMP5 were found to differ in lysates from the high fat diet model, although the role of these proteins in GLUT4 trafficking is unclear. In contrast, in the more severe diabetic db/db model GLUT4 protein content was found to be significantly reduced, but SNARE protein content was unaffected. Finally, there is also an established link between glycemic control and both the risk of developing and subsequent prognosis for myocardial infarction (MI). There is a line of evidence suggesting that cardiac insulin sensitivity may also be highly relevant in this disease context. Accordingly, it was demonstrated that cardiomyocytes isolated from a clinically relevant 8-12 weeks post-MI rabbit model exhibited impaired insulin stimulated glucose uptake. This strengthens the association between MI and cardiac metabolic parameters. However, insulin stimulated phosphorylation of Akt, GLUT4 levels, and SNARE protein expression were unaffected post-MI. Therefore future work must identify both the underlying mechanism and clinical relevance of this finding.
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Books on the topic "Cardiomyocytes"

1

Skuse, Gary R., and Maureen C. Ferran, eds. Cardiomyocytes. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2572-8.

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Michael, Piper Hans, and Isenberg Gerrit, eds. Isolated adult cardiomyocytes. Boca Raton, Fla: CRC Press, 1989.

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Skuse, Gary R., and Maureen C. Ferran. Cardiomyocytes: Methods and Protocols. New York: Humana Press, 2015.

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Yoshida, Yoshinori, ed. Pluripotent Stem-Cell Derived Cardiomyocytes. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1484-6.

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Kartha, Chandrasekharan C. Cardiomyocytes in Health and Disease. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85536-9.

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Schlüter, Klaus-Dieter, ed. Cardiomyocytes – Active Players in Cardiac Disease. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31251-4.

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Yee-Ki, Lee, and Siu Chung-Wah. Calcium Handling in hiPSC-Derived Cardiomyocytes. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4093-2.

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Luiz, Belardinelli, ed. Effects of extracellular adenosine and ATP on cardiomyocytes. Austin: Landes, 1999.

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Sowerby, Andrew John. Anoxia, plasma membrane structure and calcium homeostasis: Photobleaching and microflurescence investigations inisolated rat cardiomyocytes. Uxbridge: Brunel University, 1991.

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Lai, Laura R. B. Protein oxidation occurs in cardiomyocytes exposed to an in vitro model of hypoxia/reperfusion injury. Ottawa: National Library of Canada, 1996.

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Book chapters on the topic "Cardiomyocytes"

1

Bonci, Dèsirèe, Michael V. G. Latronico, and Gianluigi Condorelli. "Cardiomyocytes." In Lentivirus Gene Engineering Protocols, 169–79. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1385/1-59259-393-3:169.

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Thiriet, Marc. "Cardiomyocytes." In Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems, 189–269. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5966-8_5.

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Smart, F. W., W. Claycomb, J. Delcarpio, and C. Van Meter. "Cultured Cardiomyocytes." In The Transplantation and Replacement of Thoracic Organs, 775–84. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-0-585-34287-0_87.

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Kartha, Chandrasekharan C. "Cardiomyocytes in Heart Failure." In Cardiomyocytes in Health and Disease, 245–55. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85536-9_15.

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Moore, Jennifer C., Teun P. de Boer, Marcel A. G. van der Heyden, Leon G. J. Tertoolen, and Christine L. Mummery. "Stem Cells and Cardiomyocytes." In Cardiovascular Research, 133–55. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-23329-6_8.

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Szibor, Marten. "Cardiomyocytes: Function and Regeneration." In Cardiomyocytes – Active Players in Cardiac Disease, 25–65. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31251-4_2.

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Vandergriff, Adam C., M. Taylor Hensley, and Ke Cheng. "Cryopreservation of Neonatal Cardiomyocytes." In Methods in Molecular Biology, 153–60. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2572-8_12.

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Smits, Anke M., Angelique A. van Oorschot, and Marie-José Goumans. "Isolation and Differentiation of Human Cardiomyocyte Progenitor Cells into Cardiomyocytes." In Somatic Stem Cells, 339–49. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-815-3_20.

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Kartha, Chandrasekharan C. "Cell Cycle Regulation in Cardiomyocytes." In Cardiomyocytes in Health and Disease, 25–39. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85536-9_3.

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Kartha, Chandrasekharan C. "Cardiomyocyte Senescence." In Cardiomyocytes in Health and Disease, 187–205. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85536-9_12.

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Conference papers on the topic "Cardiomyocytes"

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Baicu, Catalin F., and Michael R. Zile. "Quantification of Diastolic Viscoelastic Properties of Isolated Cardiac Muscle Cells." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23158.

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Abstract Pathological processes which cause diastolic congestive heart failure (CHF), such as pressure overload hypertrophy (POH), produce abnormalities in the material properties of cardiac muscle cells (cardiomyocytes) and may selectively alter its elastic stiffness, viscosity, or both. Previous methods used to characterize these cardiomyocyte viscoelastic properties were constrained by specific biological and engineering limitations, which prevented testing in conditions that mimic normal physiology. The current study proposes an uniaxial variable-rate stretching method, in which isolated cardiomyocytes embedded in a three-dimensional gel matrix were subjected to stretch. Physiological Ca++ (2.5 mM) and rapid stretch rates up to 100 μm/sec provided experimental conditions parallel to in vivo physiology. The proposed method identified and individually quantified both cellular stiffness and viscosity, and showed that POH increased both elastic and viscous cardiomyocyte diastolic properties.
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Sargent, Carolyn Y., Luke A. Hiatt, Sandhya Anantharaman, Eric Berson, and Todd C. McDevitt. "Cardiogenesis of Embryonic Stem Cells is Modulated by Hydrodynamic Mixing Conditions." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193129.

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Embryonic stem cells (ESCs) have the potential to differentiate into all somatic cell types and are uniquely capable of differentiating into functional cardiomyocytes; however, to effectively use ESCs for cell-based therapies to regenerate viable myocardial tissue, an improved understanding of mechanisms regulating differentiation is necessary. Currently, application of exogenous factors is commonly attempted to direct stem cell differentiation; however, progression towards controlling multiple environmental factors, including biochemical and mechanical stimuli, may result in increased differentiation efficiency for clinical applications. Additionally, current methods of ESC differentiation to cardiomyocytes are labor-intensive and produce relatively few cardiomyocytes based on initial ESC densities. Rotary suspension culture to produce embryoid bodies (EBs) has been shown to yield greater numbers of differentiating ESCs than static suspension cultures [1]. Thus, the objective of this study was to examine how the hydrodynamic mixing conditions imposed by rotary orbital culture modulate cardiomyocyte differentiation.
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Liu, Honghai, Julie X. Yun, Russel K. Pirlo, Delpine Dean, Hai Yao, Martine Laberge, and Bruce Z. Gao. "The Dependence of Mechanical Properties of Adult Rat Myocytes on Cell Alignment." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193024.

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In response to damage, stress and cell death cardiac muscle undergoes remodeling in which cardiomyocytes de-differentiate and re-differentiate. An understanding of the mechanisms involved in this process may lead to therapies to promote and enhance the repair of damaged cardiac tissue. However, due to the complexity of native environments, it is hard to investigate this remodeling process directly on tissues isolated from the body. Therefore, it is important to construct a cell-culture model that will replicate the most relevant characteristics of that tissue in controlled environments with greater capability to be assessed. Native cardiac myocytes have an aligned arrangement in which neighboring cardiomyocytes are electrically and mechanical coupled through contact junctions. When adult cardiomyocytes are placed into a culture dish, the cells will be randomly oriented and lose their native phenotypes gradually due to the lack of proper aligned cell-cell connections. To address this issue, we have implemented our laser cell micropatterning system to create an adult cardiomyocyte culturing model with aligned rows of cells connected end to end. In this abstract, we describe the experimental procedure to achieve the laser alignment of adult cardiomyocytes and the results of mechanical property testing of the myocytes investigated using Multimode Picoforce Nanoscope Atomic Force Microscope (AFM) (Veeco).
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Young, Jennifer L., Kyle Kretchmer, and Adam J. Engler. "Temporally-Stiffening Hydrogel Regulates Cardiac Differentiation via Mechanosensitive Signaling." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14674.

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Stiffness of the extracellular matrix (ECM) surrounding cells plays an integral role in affecting how a cell spreads, migrates, and differentiates, in the case of stem cells. For mature cardiomyocytes, stiffness regulates myofibril striation, beating rate, and fiber alignment, but does not induce de-differentiation [1,2]. Despite improved myocyte function on materials which mimic the ∼10 kPa heart stiffness, the heart does not begin as a contractile ∼10 kPa material, but instead undergoes ∼10-fold myocardial stiffening during development [3]. Thiolated hyaluronic acid (HA) hydrogels have been used to mimic these stiffening dynamics by varying hydrogel functionality and component parameters. Recently, we have shown that pre-cardiac mesodermal cells plated on top of these stiffening HA hydrogels improves cardiomyocyte maturation compared to static, compliant polyacrylamide (PA) hydrogels [3]. While active mechanosensing causes maturation, the specific mechanisms responsible for responding to time-dependent stiffness remain unknown. Here we examined protein kinase signaling and mechanics in response to dynamic vs. static stiffness during the commitment process from embryonic stem cells (ESCs) through cardiomyocytes to better understand how developmentally-appropriate temporal changes in stiffness regulate cell commitment.
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Rodriguez, Marita L., Charles E. Murry, and Nathan J. Sniadecki. "Assessment of Induced Pluripotent Stem Cell-Derived Cardiomyocyte Contractility Using Micropost Arrays." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14640.

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Cardiovascular stem cell therapies have shown increasing promise as a potential therapeutic means for reversing the effects of a myocardial infarction [1]. Out of the currently available sources of human stem cells, human induced pluripotent stem cells (hiPSCs) are very promising in that: the number of cell lines that can be induced to the pluripotent state is extremely vast, they serve as a potential source for patient-specific cardiomyocytes, and their use is non-controversial. However, before they can be used feasibly in a clinical setting, the functional engraftment of these cells into the host tissue must be improved [2]. It is hypothesized that the structural and functional maturity of the stem-cell derived cardiomyocytes prior to implantation, may significantly affect the ability of these cells to engraft with resident heart tissue [3]. One of the most important functional characteristics of a cardiomyocyte is its ability to produce contractile forces. However, assessing the contractile properties of single iPS-CMs is a difficult task. iPS-CMs generally have relatively unorganized cytoskeletons, with stress fibers in multiple directions. This trait renders one or two-point force assays ineffectual in determining total cell forces. Furthermore, iPS-CMs don’t spread well on tissue culture surfaces, which make two-dimensional force measurements almost impossible.
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Garcia, A., M. T. Nazari-Shafti, A. Kurtz, M. Gossen, and C. Stamm. "Inducible Differentiation of iPS-Derived Cardiomyocyte Precursor Cells into Cardiomyocytes Using Biomimetic shRNA Technology." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678868.

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Williams, Brian, Sandeep Anand, Jagannathan Rajagopalan, and Taher Saif. "Artificial Swimmer Powered by Cardiomyocytes." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14854.

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We present, for the first time, a micro scale 1D swimmer powered by cardiamyocytes. It consists of a PDMS “flagella” with a head. Cardiomyocytes are plated near the head. Synchronized contraction of a small number of cells generates an elastic deformation wave in the flagella, which interacts with the fluid. Solid-fluid interaction results in a net propulsive force on the swimmer, which drives it through the fluid overcoming the drag.
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Kim, Jinseok, Sungwook Yang, Jeongeun Baek, Sewan Park, Hyeon Cheol Kim, Eui-Sung Yoon, and Kukjin Chun. "Cardiomyocytes Self-Powered Polymer Microrobot." In TRANSDUCERS 2007 - 2007 International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2007. http://dx.doi.org/10.1109/sensor.2007.4300406.

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Liu, Wenhao, Parvin Forghani, Qingyu Chen, Lawrence C. Armand, Chunhui Xu, and Shu Jia. "3D imaging of hiPSC-derived cardiomyocytes with light-field microscopy." In Frontiers in Optics. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/fio.2023.fm1e.3.

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We introduce light-field microscopy for volumetric imaging of 3D Human induced pluripotent stem cell-derived cardiomyocytes with high spatiotemporal resolution, realizing simultaneous calcium tracing and cell tracking of cardiomyocytes in 3D space and demonstrating their synchronization.
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Hurley, Jennifer R., and Daria A. Narmoneva. "Fibroblasts Induce Mechanical Changes in the Extracellular Environment and Enhance Capillary-Like Network Formation." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193093.

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Cardiac tissue engineering studies have demonstrated the importance of revascularization in engineered grafts for successful implantation and regeneration [1]. Understanding the myocardium’s complex cellular organization and the interactions between the major cardiac cell types (cardiomyocytes, endothelial cells, and cardiac fibroblasts) is critical for revascularization. Our previous studies have shown the importance of cardiomyocyte-endothelial interactions [2]. However, there is limited information available on endothelial-fibroblast interactions. We and others have previously observed that during capillary assembly, fibroblasts provide chemical signaling via expression of growth factors [3, 4]. In addition, fibroblasts may also regulate angiogenesis through alterations to the mechanical environment via myocardial remodeling, including matrix degradation and deposition, and tissue contraction. Changes to the extracellular mechanical enviroment may lead to changes in basic cell functions such as proliferation, apoptosis, and growth factor expression.
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Reports on the topic "Cardiomyocytes"

1

Pailino, Lia, Lihua Lou, Alberto Sesena Rubfiaro, Jin He, and Arvind Agarwal. Nanomechanical Properties of Engineered Cardiomyocytes Under Electrical Stimulation. Florida International University, October 2021. http://dx.doi.org/10.25148/mmeurs.009775.

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Engineered cardiomyocytes made of human-induced pluripotent stem cells (iPSC) present phenotypical characteristics similar to human fetal cardiomyocytes. There are different factors that are essential for engineered cardiomyocytes to be functional, one of them being that their mechanical properties must mimic those of adult cardiomyocytes. Techniques, such as electrical stimulation, have been used to improve the extracellular matrix's alignment and organization and improve the intracellular environment. Therefore, electrical stimulation could potentially be used to enhance the mechanical properties of engineered cardiac tissue. The goal of this study is to establish the effects of electrical stimulation on the elastic modulus of engineered cardiac tissue. Nanoindentation tests were performed on engineered cardiomyocyte constructs under seven days of electrical stimulation and engineered cardiomyocyte constructs without electrical stimulation. The tests were conducted using BioSoft™ In-Situ Indenter through displacement control mode with a 50 µm conospherical diamond fluid cell probe. The Hertzian fit model was used to analyze the data and obtain the elastic modulus for each construct. This study demonstrated that electrically stimulated cardiomyocytes (6.98 ± 0.04 kPa) present higher elastic modulus than cardiomyocytes without electrical stimulation (4.96 ± 0.29 kPa) at day 7 of maturation. These results confirm that electrical stimulation improves the maturation of cardiomyocytes. Through this study, an efficient nanoindentation method is demonstrated for engineered cardiomyocyte tissues, capable of capturing the nanomechanical differences between electrically stimulated and non-electrically stimulated cardiomyocytes.
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Gabrielson, Kathleen L. Akt Rescue in Cardiomyocytes but not Breast Cancer Cells after Doxorubicin and Anti-erbB2 Treatment. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada435439.

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liao, xiaoqian, xingyu fan, ziyi wang, shumin huang, and zhixi hu. Prognostic value of heart-type fatty acid binding protein in heart failure: a systematic review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0126.

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Review question / Objective: (1)Can heart type fatty acid binding protein effectively predict the prognosis of patients with heart failure? (2)Is high expression of ear type fat acid binding protein associated with poor clinical outcomes in patients with heart failure? Condition being studied: Heart-type fatty acid binding protein (H-FABP) mainly exists in cardiomyocytes and is a potential biomarker of myocardial injury.However, the adverse consequences of heart failure have not been fully analyzed.Therefore, the purpose of this study was to comprehensively evaluate the correlation between H-FABP and the prognosis of heart failure through meta-analysis.
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Evaluation of the utility of stem-cell derived cardiomyocytes for drug proarrhythmic potential. EMBL-EBI, March 2020. http://dx.doi.org/10.6019/chembl4295262.

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