Journal articles: 'Cardiogenesis'

1

Nascone, Nanette, and Mark Mercola. "Endoderm and Cardiogenesis." Trends in Cardiovascular Medicine 6, no. 7 (October 1996): 211–16. http://dx.doi.org/10.1016/s1050-1738(96)00086-2.

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Samuel, L. J., and B. V. Latinkic. "MHC and cardiogenesis." Development 137, no. 1 (December 18, 2009): 3. http://dx.doi.org/10.1242/dev.044917.

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3

Martin, James F., Emerson C. Perin, and James T. Willerson. "Direct Stimulation of Cardiogenesis." Circulation Research 121, no. 1 (June 23, 2017): 13–15. http://dx.doi.org/10.1161/circresaha.117.311062.

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4

Metzger, Joseph M., Linda C. Samuelson, Elizabeth M. Rust, and Margaret V. Westfall. "Embryonic Stem Cell Cardiogenesis." Trends in Cardiovascular Medicine 7, no. 2 (February 1997): 63–68. http://dx.doi.org/10.1016/s1050-1738(96)00138-7.

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Sahara, Makoto, Elif Eroglu, and Kenneth R. Chien. "Lnc’ed in to Cardiogenesis." Cell Stem Cell 22, no. 6 (June 2018): 787–89. http://dx.doi.org/10.1016/j.stem.2018.05.012.

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Muñoz-Chápuli, Ramón, and José M. Pérez-Pomares. "Cardiogenesis: An Embryological Perspective." Journal of Cardiovascular Translational Research 3, no. 1 (November 4, 2009): 37–48. http://dx.doi.org/10.1007/s12265-009-9146-1.

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7

Pucéat, Michel, and Marisa Jaconi. "Ca2+ signalling in cardiogenesis." Cell Calcium 38, no. 3-4 (September 2005): 383–89. http://dx.doi.org/10.1016/j.ceca.2005.06.016.

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Mukhopadhyay, Madhura. "Recapitulating early cardiogenesis in vitro." Nature Methods 18, no. 4 (April 2021): 331. http://dx.doi.org/10.1038/s41592-021-01118-2.

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Brade, T., L. S. Pane, A. Moretti, K. R. Chien, and K. L. Laugwitz. "Embryonic Heart Progenitors and Cardiogenesis." Cold Spring Harbor Perspectives in Medicine 3, no. 10 (October 1, 2013): a013847. http://dx.doi.org/10.1101/cshperspect.a013847.

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Fougerousse, Françoise, Louise V. B. Anderson, Anne-Lise Delezoide, Laurence Suel, Muriel Durand, and Jacques S. Beckmann. "Calpain3 expression during human cardiogenesis." Neuromuscular Disorders 10, no. 4-5 (June 2000): 251–56. http://dx.doi.org/10.1016/s0960-8966(99)00107-8.

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Mohun, Tim, and Duncan Sparrow. "Early steps in vertebrate cardiogenesis." Current Opinion in Genetics & Development 7, no. 5 (October 1997): 628–33. http://dx.doi.org/10.1016/s0959-437x(97)80010-x.

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12

Niu, Zhivy, Ankang Li, Shu X. Zhang, and Robert J. Schwartz. "Serum response factor micromanaging cardiogenesis." Current Opinion in Cell Biology 19, no. 6 (December 2007): 618–27. http://dx.doi.org/10.1016/j.ceb.2007.09.013.

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13

Sweeney, L. J. "A molecular view of cardiogenesis." Experientia 44, no. 11-12 (December 1988): 930–36. http://dx.doi.org/10.1007/bf01939886.

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14

ROBBINS, J. "The murine model of cardiogenesis." Journal of Molecular and Cellular Cardiology 23 (April 1991): S9. http://dx.doi.org/10.1016/0022-2828(91)91350-z.

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15

Li, Xing, Almudena Martinez-Fernandez, Katherine A. Hartjes, Jean-Pierre A. Kocher, Timothy M. Olson, Andre Terzic, and Timothy J. Nelson. "Transcriptional atlas of cardiogenesis maps congenital heart disease interactome." Physiological Genomics 46, no. 13 (July 1, 2014): 482–95. http://dx.doi.org/10.1152/physiolgenomics.00015.2014.

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Mammalian heart development is built on highly conserved molecular mechanisms with polygenetic perturbations resulting in a spectrum of congenital heart diseases (CHD). However, knowledge of cardiogenic ontogeny that regulates proper cardiogenesis remains largely based on candidate-gene approaches. Mapping the dynamic transcriptional landscape of cardiogenesis from a genomic perspective is essential to integrate the knowledge of heart development into translational applications that accelerate disease discovery efforts toward mechanistic-based treatment strategies. Herein, we designed a time-course transcriptome analysis to investigate the genome-wide dynamic expression landscape of innate murine cardiogenesis ranging from embryonic stem cells to adult cardiac structures. This comprehensive analysis generated temporal and spatial expression profiles, revealed stage-specific gene functions, and mapped the dynamic transcriptome of cardiogenesis to curated pathways. Reconciling known genetic underpinnings of CHD, we deconstructed a disease-centric dynamic interactome encoded within this cardiogenic atlas to identify stage-specific developmental disturbances clustered on regulation of epithelial-to-mesenchymal transition (EMT), BMP signaling, NF-AT signaling, TGFb-dependent EMT, and Notch signaling. Collectively, this cardiogenic transcriptional landscape defines the time-dependent expression of cardiac ontogeny and prioritizes regulatory networks at the interface between health and disease.

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Lim, Tingsen Benson, Sik Yin Roger Foo, and Ching Kit Chen. "The Role of Epigenetics in Congenital Heart Disease." Genes 12, no. 3 (March 9, 2021): 390. http://dx.doi.org/10.3390/genes12030390.

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Congenital heart disease (CHD) is the most common birth defect among newborns worldwide and contributes to significant infant morbidity and mortality. Owing to major advances in medical and surgical management, as well as improved prenatal diagnosis, the outcomes for these children with CHD have improved tremendously so much so that there are now more adults living with CHD than children. Advances in genomic technologies have discovered the genetic causes of a significant fraction of CHD, while at the same time pointing to remarkable complexity in CHD genetics. For this reason, the complex process of cardiogenesis, which is governed by multiple interlinked and dose-dependent pathways, is a well investigated process. In addition to the sequence of the genome, the contribution of epigenetics to cardiogenesis is increasingly recognized. Significant progress has been made dissecting the epigenome of the heart and identified associations with cardiovascular diseases. The role of epigenetic regulation in cardiac development/cardiogenesis, using tissue and animal models, has been well reviewed. Here, we curate the current literature based on studies in humans, which have revealed associated and/or causative epigenetic factors implicated in CHD. We sought to summarize the current knowledge on the functional role of epigenetics in cardiogenesis as well as in distinct CHDs, with an aim to provide scientists and clinicians an overview of the abnormal cardiogenic pathways affected by epigenetic mechanisms, for a better understanding of their impact on the developing fetal heart, particularly for readers interested in CHD research.

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Mignone, John L., Kareen L. Kreutziger, Sharon L. Paige, and Charles E. Murry. "Cardiogenesis From Human Embryonic Stem Cells." Circulation Journal 74, no. 12 (2010): 2517–26. http://dx.doi.org/10.1253/circj.cj-10-0958.

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18

Pentecost, Jeffrey O., Jose Icardo, and Kent L. Thornburg. "3D Computer modeling of human cardiogenesis." Computerized Medical Imaging and Graphics 23, no. 1 (January 1999): 45–49. http://dx.doi.org/10.1016/s0895-6111(98)00063-9.

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19

Dupays, Laurent, and Timothy Mohun. "Spatiotemporal regulation of enhancers during cardiogenesis." Cellular and Molecular Life Sciences 74, no. 2 (August 6, 2016): 257–65. http://dx.doi.org/10.1007/s00018-016-2322-y.

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Brand, Marcus, Hervé Kempf, Martin Paul, Pierre Corvol, and Jean-Marie Gasc. "Expression of endothelins in human cardiogenesis." Journal of Molecular Medicine 80, no. 11 (November 1, 2002): 715–23. http://dx.doi.org/10.1007/s00109-002-0379-6.

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21

Cai, Jingzeng, Jie Yang, Qi Liu, Yafan Gong, Yuan Zhang, and Ziwei Zhang. "Selenium deficiency inhibits myocardial development and differentiation by targeting the mir-215-5p/CTCF axis in chicken." Metallomics 11, no. 2 (2019): 415–28. http://dx.doi.org/10.1039/c8mt00319j.

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22

Piven, Oksana O., and Cecilia L. Winata. "The canonical way to make a heart: β-catenin and plakoglobin in heart development and remodeling." Experimental Biology and Medicine 242, no. 18 (September 18, 2017): 1735–45. http://dx.doi.org/10.1177/1535370217732737.

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The main mediator of the canonical Wnt pathway, β-catenin, is a major effector of embryonic development, postnatal tissue homeostasis, and adult tissue regeneration. The requirement for β-catenin in cardiogenesis and embryogenesis has been well established. However, many questions regarding the molecular mechanisms by which β-catenin and canonical Wnt signaling regulate these developmental processes remain unanswered. An interesting question that emerged from our studies concerns how β-catenin signaling is modulated through interaction with other factors. Recent experimental data implicate new players in canonical Wnt signaling, particularly those which modulate β-catenin function in many its biological processes, including cardiogenesis. One of the interesting candidates is plakoglobin, a little-studied member of the catenin family which shares several mechanistic and functional features with its close relative, β-catenin. Here we have focused on the function of β-catenin in cardiogenesis. We also summarize findings on plakoglobin signaling function and discuss possible interplays between β-catenin and plakoglobin in the regulation of embryonic heart development. Impact statement Heart development, function, and remodeling are complex processes orchestrated by multiple signaling networks. This review examines our current knowledge of the role of canonical Wnt signaling in cardiogenesis and heart remodeling, focusing primarily on the mechanistic action of its effector β-catenin. We summarize the generally accepted understanding of the field based on experimental in vitro and in vivo data, and address unresolved questions in the field, specifically relating to the role of canonical Wnt signaling in heart maturation and regeneration. What are the modulators of canonical Wnt, and particularly what are the potential roles of plakoglobin, a close relative of β-catenin, in regulating Wnt signaling?Answers to these questions will enhance our understanding of the mechanism by which the canonical Wnt signaling regulates development of the heart and its regeneration after damage.

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23

Alsan, Burak H., and Thomas M. Schultheiss. "Regulation of avian cardiogenesis by Fgf8 signaling." Development 129, no. 8 (April 15, 2002): 1935–43. http://dx.doi.org/10.1242/dev.129.8.1935.

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The avian heart develops from paired primordia located in the anterior lateral mesoderm of the early embryo. Previous studies have found that the endoderm adjacent to the cardiac primordia plays an important role in heart specification. The current study provides evidence that fibroblast growth factor (Fgf) signaling contributes to the heart-inducing properties of the endoderm. Fgf8 is expressed in the endoderm adjacent to the precardiac mesoderm. Removal of endoderm results in a rapid downregulation of a subset of cardiac markers, including Nkx2.5 and Mef2c. Expression of these markers can be rescued by supplying exogenous Fgf8. In addition, application of ectopic Fgf8 results in ectopic expression of cardiac markers. Expression of cardiac markers is expanded only in regions where bone morphogenetic protein (Bmp) signaling is also present, suggesting that cardiogenesis occurs in regions exposed to both Fgf and Bmp signaling. Finally, evidence is presented that Fgf8 expression is regulated by particular levels of Bmp signaling. Application of low concentrations of Bmp2 results in ectopic expression of Fgf8, while application of higher concentrations of Bmp2 result in repression of Fgf8 expression. Together, these data indicate that Fgf signaling cooperates with Bmp signaling to regulate early cardiogenesis.

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24

KIRBY, MARGARET L. "Alteration of Cardiogenesis after Neural Crest Ablation." Annals of the New York Academy of Sciences 588, no. 1 Embryonic Ori (April 1990): 289–95. http://dx.doi.org/10.1111/j.1749-6632.1990.tb13218.x.

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25

Franco, D., and R. G. Kelly. "Contemporary cardiogenesis: new insights into heart development." Cardiovascular Research 91, no. 2 (June 1, 2011): 183–84. http://dx.doi.org/10.1093/cvr/cvr160.

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26

Williams, Ruth. "Margaret Buckingham: Studying the Choreography of Cardiogenesis." Circulation Research 110, no. 6 (March 16, 2012): 805–7. http://dx.doi.org/10.1161/res.0b013e3182507c49.

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27

Schneider, V. A. "Wnt antagonism initiates cardiogenesis in Xenopus laevis." Genes & Development 15, no. 3 (February 1, 2001): 304–15. http://dx.doi.org/10.1101/gad.855601.

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28

Stefanovic, Sonia, and Stéphane Zaffran. "Mechanisms of retinoic acid signaling during cardiogenesis." Mechanisms of Development 143 (February 2017): 9–19. http://dx.doi.org/10.1016/j.mod.2016.12.002.

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29

Pedrazzini, Thierry. "Control of Cardiogenesis by the Notch Pathway." Trends in Cardiovascular Medicine 17, no. 3 (April 2007): 83–90. http://dx.doi.org/10.1016/j.tcm.2007.01.003.

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30

McNally, Elizabeth, and Lisa Dellefave. "Sarcomere Mutations in Cardiogenesis and Ventricular Noncompaction." Trends in Cardiovascular Medicine 19, no. 1 (January 2009): 17–21. http://dx.doi.org/10.1016/j.tcm.2009.03.003.

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31

Li, Yan, Xiaoyu Wang, Zhenglai Ma, Manli Chuai, Andrea Münsterberg, Kenneth KaHo Lee, and Xuesong Yang. "Endoderm contributes to endocardial composition during cardiogenesis." Chinese Science Bulletin 59, no. 22 (May 20, 2014): 2749–55. http://dx.doi.org/10.1007/s11434-014-0366-7.

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32

Lombó, Marta, and María Paz Herráez. "Paternal Inheritance of Bisphenol A Cardiotoxic Effects: The Implications of Sperm Epigenome." International Journal of Molecular Sciences 22, no. 4 (February 20, 2021): 2125. http://dx.doi.org/10.3390/ijms22042125.

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Parental exposure to bisphenol A (BPA) has been linked to a greater incidence of congenital diseases. We have demonstrated that BPA induces in zebrafish males an increase in the acetylation of sperm histones that is transmitted to the blastomeres of the unexposed progeny. This work is aimed to determine whether histone hyperacetylation promoted by paternal exposure to BPA is the molecular mechanism underlying the cardiogenesis impairment in the descendants. Zebrafish males were exposed to 100 and 2000 µg/L BPA during early spermatogenesis and mated with non-exposed females. We analyzed in the progeny the expression of genes involved in cardiogenesis and the epigenetic profile. Once the histone hyperacetylation was confirmed, treatment with epigallocatechin gallate (EGCG), an inhibitor of histone acetyltransferases, was assayed on F1 embryos. Embryos from males exposed to 2000 µg/L BPA overexpressed the transcription factor hand2 and the receptor esr2b, showing their own promoters—as well as that of kat6a—an enrichment in H3K9ac. In embryos treated with EGCG, both gene expression and histone acetylation (global and specific) returned to basal levels, and the phenotype was recovered. As shown by the results, the histone hyperacetylated landscape promoted by BPA in the sperm alters the chromatin structure of the progeny, leading to the overexpression of the histone acetyltransferase and genes involved in cardiogenesis.

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Hoelscher, Sarah C., Theresia Stich, Anne Diehm, Harald Lahm, Martina Dreßen, Zhong Zhang, Irina Neb, et al. "miR-128a Acts as a Regulator in Cardiac Development by Modulating Differentiation of Cardiac Progenitor Cell Populations." International Journal of Molecular Sciences 21, no. 3 (February 10, 2020): 1158. http://dx.doi.org/10.3390/ijms21031158.

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MicroRNAs (miRs) appear to be major, yet poorly understood players in regulatory networks guiding cardiogenesis. We sought to identify miRs with unknown functions during cardiogenesis analyzing the miR-profile of multipotent Nkx2.5 enhancer cardiac progenitor cells (NkxCE-CPCs). Besides well-known candidates such as miR-1, we found about 40 miRs that were highly enriched in NkxCE-CPCs, four of which were chosen for further analysis. Knockdown in zebrafish revealed that only miR-128a affected cardiac development and function robustly. For a detailed analysis, loss-of-function and gain-of-function experiments were performed during in vitro differentiations of transgenic murine pluripotent stem cells. MiR-128a knockdown (1) increased Isl1, Sfrp5, and Hcn4 (cardiac transcription factors) but reduced Irx4 at the onset of cardiogenesis, (2) upregulated Isl1-positive CPCs, whereas NkxCE-positive CPCs were downregulated, and (3) increased the expression of the ventricular cardiomyocyte marker Myl2 accompanied by a reduced beating frequency of early cardiomyocytes. Overexpression of miR-128a (4) diminished the expression of Isl1, Sfrp5, Nkx2.5, and Mef2c, but increased Irx4, (5) enhanced NkxCE-positive CPCs, and (6) favored nodal-like cardiomyocytes (Tnnt2+, Myh6+, Shox2+) accompanied by increased beating frequencies. In summary, we demonstrated that miR-128a plays a so-far unknown role in early heart development by affecting the timing of CPC differentiation into various cardiomyocyte subtypes.

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34

Hofbauer, Pablo, Stefan M. Jahnel, Nora Papai, Magdalena Giesshammer, Alison Deyett, Clara Schmidt, Mirjam Penc, et al. "Cardioids reveal self-organizing principles of human cardiogenesis." Cell 184, no. 12 (June 2021): 3299–317. http://dx.doi.org/10.1016/j.cell.2021.04.034.

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35

Lozano-Velasco, Estefania, Carlos Garcia-Padilla, Maria del Mar Muñoz-Gallardo, Francisco Jose Martinez-Amaro, Sheila Caño-Carrillo, Juan Manuel Castillo-Casas, Cristina Sanchez-Fernandez, Amelia E. Aranega, and Diego Franco. "Post-Transcriptional Regulation of Molecular Determinants during Cardiogenesis." International Journal of Molecular Sciences 23, no. 5 (March 4, 2022): 2839. http://dx.doi.org/10.3390/ijms23052839.

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Cardiovascular development is initiated soon after gastrulation as bilateral precardiac mesoderm is progressively symmetrically determined at both sides of the developing embryo. The precardiac mesoderm subsequently fused at the embryonic midline constituting an embryonic linear heart tube. As development progress, the embryonic heart displays the first sign of left-right asymmetric morphology by the invariably rightward looping of the initial heart tube and prospective embryonic ventricular and atrial chambers emerged. As cardiac development progresses, the atrial and ventricular chambers enlarged and distinct left and right compartments emerge as consequence of the formation of the interatrial and interventricular septa, respectively. The last steps of cardiac morphogenesis are represented by the completion of atrial and ventricular septation, resulting in the configuration of a double circuitry with distinct systemic and pulmonary chambers, each of them with distinct inlets and outlets connections. Over the last decade, our understanding of the contribution of multiple growth factor signaling cascades such as Tgf-beta, Bmp and Wnt signaling as well as of transcriptional regulators to cardiac morphogenesis have greatly enlarged. Recently, a novel layer of complexity has emerged with the discovery of non-coding RNAs, particularly microRNAs and lncRNAs. Herein, we provide a state-of-the-art review of the contribution of non-coding RNAs during cardiac development. microRNAs and lncRNAs have been reported to functional modulate all stages of cardiac morphogenesis, spanning from lateral plate mesoderm formation to outflow tract septation, by modulating major growth factor signaling pathways as well as those transcriptional regulators involved in cardiac development.

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36

Heallen, Todd R., Zachary A. Kadow, Jong H. Kim, Jun Wang, and James F. Martin. "Stimulating Cardiogenesis as a Treatment for Heart Failure." Circulation Research 124, no. 11 (May 24, 2019): 1647–57. http://dx.doi.org/10.1161/circresaha.118.313573.

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37

Srivastava, Deepak. "GENETIC REGULATION OF CARDIOGENESIS AND CONGENITAL HEART DISEASE." Annual Review of Pathology: Mechanisms of Disease 1, no. 1 (February 2006): 199–213. http://dx.doi.org/10.1146/annurev.pathol.1.110304.100039.

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38

Mironov, Vladimir, Richard P. Visconti, and Roger R. Markwald. "On the Role of Shear Stress in Cardiogenesis." Endothelium 12, no. 5-6 (January 2005): 259–61. http://dx.doi.org/10.1080/10623320500476708.

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39

Raddatz, E., M. Servin, and P. Kucera. "Oxygen uptake during early cardiogenesis of the chick." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 4 (April 1, 1992): H1224—H1230. http://dx.doi.org/10.1152/ajpheart.1992.262.4.h1224.

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Oxidative metabolism of the isolated embryonic heart of the chick has been determined using a spectrophotometric technique allowing global as well as localized micromeasurements of the O2 uptake. Entire hearts, excised from embryos of 10 somites (primordia fused, stage 10 HH) and 40 somites (S shaped, stage 20 HH) were placed in a special chamber under controlled metabolic conditions where they continued to beat spontaneously and regularly. During the 32 h of development, the O2 consumption of the whole heart increased from 0.9 +/- 0.1 to 5.3 +/- 0.8 nmol O2/h. These values corrected for protein content were, however, comparable (0.45 nmol O2.h-1.micrograms-1). At stage 10-12, the O2 uptake varied along the cardiac tube (from 0.74 to 1.0 nmol O2.h-1.mm-2). From stage 10 to 20, the O2 uptake per unit area of ventricle wall increased from 0.7 +/- 0.2 to 1.8 +/- 0.2 nmol O2.h-1.mm-2, and the O2 uptake per myocardial volume during one cardiac cycle varied from 7 to 2.5 nmol O2/cm3. These results indicate that, despite an intense morphogenesis, the cardiac tissue has a rather low and stable oxidative metabolism, although the O2 requirement of the whole heart increases significantly. Moreover, the normalized suprabasal aerobic energy expenditure decreases throughout early cardiogenesis. The functional integrity of the isolated embryonic heart combined with the experimental possibilities of the microtechnique make the preparation appropriate for studying the changes in cardiac metabolism during development.

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Yamak, A., B. V. Latinkic, R. Dali, R. Temsah, and M. Nemer. "Cyclin D2 is a GATA4 cofactor in cardiogenesis." Proceedings of the National Academy of Sciences 111, no. 4 (January 13, 2014): 1415–20. http://dx.doi.org/10.1073/pnas.1312993111.

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41

WOZNIEWICZ, B. "340 Heart failure and de novo human cardiogenesis." European Journal of Heart Failure Supplements 3, no. 1 (June 2004): 85–86. http://dx.doi.org/10.1016/s1567-4215(04)90250-0.

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42

Wu, Mingfu. "Mechanisms of Trabecular Formation and Specification During Cardiogenesis." Pediatric Cardiology 39, no. 6 (March 28, 2018): 1082–89. http://dx.doi.org/10.1007/s00246-018-1868-x.

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43

Artap, Stanley, Lauren J. Manderfield, Cheryl L. Smith, Andrey Poleshko, Haig Aghajanian, Kelvin See, Li Li, Rajan Jain, and Jonathan A. Epstein. "Endocardial Hippo signaling regulates myocardial growth and cardiogenesis." Developmental Biology 440, no. 1 (August 2018): 22–30. http://dx.doi.org/10.1016/j.ydbio.2018.04.026.

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44

Zhang, Chi, Tamara Basta, and Michael W. Klymkowsky. "SOX7 and SOX18 are essential for cardiogenesis inXenopus." Developmental Dynamics 234, no. 4 (December 2005): 878–91. http://dx.doi.org/10.1002/dvdy.20565.

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45

Robbins, Jeffrey, Thomas Doetschman, W. Keith Jones, and Alejandro Sánchez. "Embryonic stem cells as a model for cardiogenesis." Trends in Cardiovascular Medicine 2, no. 2 (March 1992): 44–50. http://dx.doi.org/10.1016/1050-1738(92)90003-b.

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46

BEHFAR, A., C. PEREZTERZIC, D. HODGSON, A. ALEKSEEV, G. KANE, M. PUCEAT, and A. TERZIC. "Guided cardiogenesis for safe stem cell-based therapy." Clinical Pharmacology & Therapeutics 77, no. 2 (February 2005): P3. http://dx.doi.org/10.1016/j.clpt.2004.11.015.

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Hatcher, Cathy J., Min-Su Kim, Caroline S. Mah, Marsha M. Goldstein, Benjamin Wong, Takashi Mikawa, and Craig T. Basson. "TBX5 Transcription Factor Regulates Cell Proliferation during Cardiogenesis." Developmental Biology 230, no. 2 (February 2001): 177–88. http://dx.doi.org/10.1006/dbio.2000.0134.

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48

Klug, M. G., M. H. Soonpaa, and L. J. Field. "DNA synthesis and multinucleation in embryonic stem cell-derived cardiomyocytes." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 6 (December 1, 1995): H1913—H1921. http://dx.doi.org/10.1152/ajpheart.1995.269.6.h1913.

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The proliferative capacity of embryonic stem (ES) cell-derived cardiomyocytes was assessed. Enriched preparations of cardiomyocytes were isolated by microdissection of the cardiogenic regions of cultured embryoid bodies. The identity of the isolated cells was established by immunocytology, and mitotic activity was monitored by [3H]thymidine incorporation and pulse-chase experiments. ES-derived cardiomyocytes were mitotically active and predominantly mononucleated at 11 days after cardiogenic induction. By 21 days postinduction, cardiomyocyte DNA synthesis was markedly decreased, with a concomitant increase in the percentage of multinucleated cells. Interestingly, the duration of active cardiomyocyte reduplication in the ES system appeared to be roughly similar to that observed during normal murine cardiogenesis. Given these observations, as well as the genetic tractability of ES cells, ES-derived cardiogenesis might provide a useful in vitro system with which to assess the molecular regulation of the cardiomyocyte cell cycle.

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Martin, Kendall E., and Joshua S. Waxman. "Atrial and Sinoatrial Node Development in the Zebrafish Heart." Journal of Cardiovascular Development and Disease 8, no. 2 (February 9, 2021): 15. http://dx.doi.org/10.3390/jcdd8020015.

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Proper development and function of the vertebrate heart is vital for embryonic and postnatal life. Many congenital heart defects in humans are associated with disruption of genes that direct the formation or maintenance of atrial and pacemaker cardiomyocytes at the venous pole of the heart. Zebrafish are an outstanding model for studying vertebrate cardiogenesis, due to the conservation of molecular mechanisms underlying early heart development, external development, and ease of genetic manipulation. Here, we discuss early developmental mechanisms that instruct appropriate formation of the venous pole in zebrafish embryos. We primarily focus on signals that determine atrial chamber size and the specialized pacemaker cells of the sinoatrial node through directing proper specification and differentiation, as well as contemporary insights into the plasticity and maintenance of cardiomyocyte identity in embryonic zebrafish hearts. Finally, we integrate how these insights into zebrafish cardiogenesis can serve as models for human atrial defects and arrhythmias.

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Méry, Annabelle, Franck Aimond, Claudine Ménard, Katsuhiko Mikoshiba, Marek Michalak, and Michel Pucéat. "Initiation of Embryonic Cardiac Pacemaker Activity by Inositol 1,4,5-Trisphosphate–dependent Calcium Signaling." Molecular Biology of the Cell 16, no. 5 (May 2005): 2414–23. http://dx.doi.org/10.1091/mbc.e04-10-0883.

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In the adult, the heart rate is driven by spontaneous and repetitive depolarizations of pacemaker cells to generate a firing of action potentials propagating along the conduction system and spreading into the ventricles. In the early embryo before E9.5, the pacemaker ionic channel responsible for the spontaneous depolarization of cells is not yet functional. Thus the mechanisms that initiate early heart rhythm during cardiogenesis are puzzling. In the absence of a functional pacemaker ionic channel, the oscillatory nature of inositol 1,4,5-trisphosphate (InsP3)-induced intracellular Ca2+ signaling could provide an alternative pacemaking mechanism. To test this hypothesis, we have engineered pacemaker cells from embryonic stem (ES) cells, a model that faithfully recapitulates early stages of heart development. We show that InsP3-dependent shuttle of free Ca2+ in and out of the endoplasmic reticulum is essential for a proper generation of pacemaker activity during early cardiogenesis and fetal life.

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Journal articles on the topic 'Cardiogenesis'

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