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Journal articles on the topic 'Cardiomyogenesis'

To see the other types of publications on this topic, follow the link: Cardiomyogenesis.

Author: Grafiati

Published: 4 June 2021

Last updated: 19 February 2023

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1

Gomez, José A., Alan Payne, Richard E. Pratt, Conrad P. Hodgkinson, and Victor J. Dzau. "A role for Sfrp2 in cardiomyogenesis in vivo." Proceedings of the National Academy of Sciences 118, no. 33 (August 11, 2021): e2103676118. http://dx.doi.org/10.1073/pnas.2103676118.

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Cardiomyogenesis, the process by which the body generates cardiomyocytes, is poorly understood. We have recently shown that Sfrp2 promotes cardiomyogenesis in vitro. The objective of this study was to determine if Sfrp2 would similarly promote cardiomyogenesis in vivo. To test this hypothesis, we tracked multipotent cKit(+) cells in response to Sfrp2 treatment. In control adult mice, multipotent cKit(+) cells typically differentiated into endothelial cells but not cardiomyocytes. In contrast, Sfrp2 switched the fate of these cells. Following Sfrp2 injection, multipotent cKit(+) cells differentiated solely into cardiomyocytes. Sfrp2-derived cardiomyocytes integrated into the myocardium and exhibited identical physiological properties to preexisting native cardiomyocytes. The ability of Sfrp2 to promote cardiomyogenesis was further supported by tracking EdU-labeled cells. In addition, Sfrp2 did not promote the formation of new cardiomyocytes when the cKit(+) cell population was selectively ablated in vivo using a diphtheria toxin receptor–diphtheria toxin model. Notably, Sfrp2-induced cardiomyogenesis was associated with significant functional improvements in a cardiac injury model. In summary, our study further demonstrates the importance of Sfrp2 in cardiomyogenesis.

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Li, Haobo, Lena E. Trager, Xiaojun Liu, Margaret H. Hastings, Chunyang Xiao, Justin Guerra, Samantha To, et al. "lncExACT1 and DCHS2 Regulate Physiological and Pathological Cardiac Growth." Circulation 145, no. 16 (April 19, 2022): 1218–33. http://dx.doi.org/10.1161/circulationaha.121.056850.

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Background: The heart grows in response to pathological and physiological stimuli. The former often precedes cardiomyocyte loss and heart failure; the latter paradoxically protects the heart and enhances cardiomyogenesis. The mechanisms underlying these differences remain incompletely understood. Although long noncoding RNAs (lncRNAs) are important in cardiac development and disease, less is known about their roles in physiological hypertrophy or cardiomyogenesis. Methods: RNA sequencing was applied to hearts from mice after 8 weeks of voluntary exercise-induced physiological hypertrophy and cardiomyogenesis or transverse aortic constriction for 2 or 8 weeks to induce pathological hypertrophy or heart failure. The top lncRNA candidate was overexpressed in hearts with adeno-associated virus vectors and inhibited with antisense locked nucleic acid–GapmeRs to examine its function. Downstream effectors were identified through promoter analyses and binding assays. The functional roles of a novel downstream effector, dachsous cadherin-related 2 (DCHS2), were examined through transgenic overexpression in zebrafish and cardiac-specific deletion in Cas9-knockin mice. Results: We identified exercise-regulated cardiac lncRNAs, called lncExACTs. lncExACT1 was evolutionarily conserved and decreased in exercised hearts but increased in human and experimental heart failure. Cardiac lncExACT1 overexpression caused pathological hypertrophy and heart failure; lncExACT1 inhibition induced physiological hypertrophy and cardiomyogenesis, protecting against cardiac fibrosis and dysfunction. lncExACT1 functioned by regulating microRNA-222, calcineurin signaling, and Hippo/Yap1 signaling through DCHS2. Cardiomyocyte DCHS2 overexpression in zebrafish induced pathological hypertrophy and impaired cardiac regeneration, promoting scarring after injury. In contrast, murine DCHS2 deletion induced physiological hypertrophy and promoted cardiomyogenesis. Conclusions: These studies identify lncExACT1-DCHS2 as a novel pathway regulating cardiac hypertrophy and cardiomyogenesis. lncExACT1-DCHS2 acts as a master switch toggling the heart between physiological and pathological growth to determine functional outcomes, providing a potentially tractable therapeutic target for harnessing the beneficial effects of exercise.

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Sepac, Ana, Zeljko J. Bosnjak, Sven Seiwerth, Suncana Sikiric, Tihana Regovic Dzombeta, Ana Kulic, Jelena Marunica Karsaj, and Filip Sedlic. "Human C2a and C6a iPSC lines and H9 ESC line have less efficient cardiomyogenesis than H1 ESC line: Beating enhances cardiac differentiation." International Journal of Developmental Biology 65, no. 10-11-12 (2021): 537–43. http://dx.doi.org/10.1387/ijdb.210115fs.

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Background: Human induced pluripotent stem cells (hiPSCs) need to be thoroughly characterized to exploit their potential advantages in various aspects of biomedicine. The aim of this study was to compare the efficiency of cardiomyogenesis of two hiPSCs and two human embryonic stem cell (hESC) lines by genetic living cardiomyocyte labeling. We also analyzed the influence of spontaneous beating on cardiac differentiation. Methods: H1 and H9 hESC lines and C2a and C6a hiPSC lines were induced into in vitro directed cardiac differentiation. Cardiomyogenesis was evaluated by the analysis of cell cluster beating, cardiac protein expression by immunocytochemistry, ability of cells to generate calcium transients, and cardiomyocyte quantification by the myosin light chain 2v-enhanced green fluorescent protein gene construct delivered with a lentiviral vector. Results: Differentiation of all cell lines yielded spontaneously beating cell clusters, indicating the presence of functional cardiomyocytes. After the cell dissociation, H1-hESC-derived cardiomyocytes exhibited spontaneous calcium transients, corresponding to autonomous electrical activity and displayed ability to transmit them between the cells. Differentiated hESC and hiPSC cells exhibited striated sarcomeres and expressed cardiac proteins sarcomeric α-actinin and cardiac troponin T. Cardiomyocytes were the most abundant in differentiated H1 hESC line (20% more than in other tested lines). In all stem cell lines, cardiomyocyte enrichment was greater in beating than in non-beating cell clusters, irrespective of cardiomyogenesis efficiency. Conclusion: Although C2a and C6a hiPSC and H9 hESC lines exhibited efficient cardiomyogenesis, H1 hESC line yielded the greatest cardiomyocyte enrichment of all tested lines. Beating of cell clusters promotes cardiomyogenesis in tested hESCs and hiPSCs.

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4

Lerchenmüller, Carolin, Ana Vujic, Sonja Mittag, Annie Wang, Charles P. Rabolli, Chiara Heß, Fynn Betge, et al. "Restoration of Cardiomyogenesis in Aged Mouse Hearts by Voluntary Exercise." Circulation 146, no. 5 (August 2, 2022): 412–26. http://dx.doi.org/10.1161/circulationaha.121.057276.

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Background: The human heart has limited capacity to generate new cardiomyocytes and this capacity declines with age. Because loss of cardiomyocytes may contribute to heart failure, it is crucial to explore stimuli of endogenous cardiac regeneration to favorably shift the balance between loss of cardiomyocytes and the birth of new cardiomyocytes in the aged heart. We have previously shown that cardiomyogenesis can be activated by exercise in the young adult mouse heart. Whether exercise also induces cardiomyogenesis in aged hearts, however, is still unknown. Here, we aim to investigate the effect of exercise on the generation of new cardiomyocytes in the aged heart. Methods: Aged (20-month-old) mice were subjected to an 8-week voluntary running protocol, and age-matched sedentary animals served as controls. Cardiomyogenesis in aged hearts was assessed on the basis of 15 N-thymidine incorporation and multi-isotope imaging mass spectrometry. We analyzed 1793 cardiomyocytes from 5 aged sedentary mice and compared these with 2002 cardiomyocytes from 5 aged exercised mice, followed by advanced histology and imaging to account for ploidy and nucleation status of the cell. RNA sequencing and subsequent bioinformatic analyses were performed to investigate transcriptional changes induced by exercise specifically in aged hearts in comparison with young hearts. Results: Cardiomyogenesis was observed at a significantly higher frequency in exercised compared with sedentary aged hearts on the basis of the detection of mononucleated/diploid 15 N-thymidine–labeled cardiomyocytes. No mononucleated/diploid 15 N-thymidine–labeled cardiomyocyte was detected in sedentary aged mice. The annual rate of mononucleated/diploid 15 N-thymidine–labeled cardiomyocytes in aged exercised mice was 2.3% per year. This compares with our previously reported annual rate of 7.5% in young exercised mice and 1.63% in young sedentary mice. Transcriptional profiling of young and aged exercised murine hearts and their sedentary controls revealed that exercise induces pathways related to circadian rhythm, irrespective of age. One known oscillating transcript, however, that was exclusively upregulated in aged exercised hearts, was isoform 1.4 of regulator of calcineurin, whose regulation and functional role were explored further. Conclusions: Our data demonstrate that voluntary running in part restores cardiomyogenesis in aged mice and suggest that pathways associated with circadian rhythm may play a role in physiologically stimulated cardiomyogenesis.

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5

Yasuda, Satoshi, Tetsuya Hasegawa, Tetsuji Hosono, Mitsutoshi Satoh, Kei Watanabe, Kageyoshi Ono, Shunichi Shimizu, et al. "AW551984: a novel regulator of cardiomyogenesis in pluripotent embryonic cells." Biochemical Journal 437, no. 2 (June 28, 2011): 345–55. http://dx.doi.org/10.1042/bj20110520.

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An understanding of the mechanism that regulates the cardiac differentiation of pluripotent stem cells is necessary for the effective generation and expansion of cardiomyocytes as cell therapy products. In the present study, we have identified genes that modulate the cardiac differentiation of pluripotent embryonic cells. We isolated P19CL6 cell sublines that possess distinct properties in cardiomyogenesis and extracted 24 CMR (cardiomyogenesis-related candidate) genes correlated with cardiomyogenesis using a transcriptome analysis. Knockdown of the CMR genes by RNAi (RNA interference) revealed that 18 genes influence spontaneous contraction or transcript levels of cardiac marker genes in EC (embryonal carcinoma) cells. We also performed knockdown of the CMR genes in mouse ES (embryonic stem) cells and induced in vitro cardiac differentiation. Three CMR genes, AW551984, 2810405K02Rik (RIKEN cDNA 2810405K02 gene) and Cd302 (CD302 antigen), modulated the cardiac differentiation of both EC cells and ES cells. Depletion of AW551984 attenuated the expression of the early cardiac transcription factor Nkx2.5 (NK2 transcription factor related locus 5) without affecting transcript levels of pluripotency and early mesoderm marker genes during ES cell differentiation. Activation of Wnt/β-catenin signalling enhanced the expression of both AW551984 and Nkx2.5 in ES cells during embryoid body formation. Our findings indicate that AW551984 is a novel regulator of cardiomyogenesis from pluripotent embryonic cells, which links Wnt/β-catenin signalling to Nkx2.5 expression.

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6

Kajstura, Jan, Konrad Urbanek, Shira Perl, Toru Hosoda, Hanqiao Zheng, Barbara Ogórek, João Ferreira-Martins, et al. "Cardiomyogenesis in the Adult Human Heart." Circulation Research 107, no. 2 (July 23, 2010): 305–15. http://dx.doi.org/10.1161/circresaha.110.223024.

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7

Habib, Manhal, Oren Caspi, and Lior Gepstein. "Human embryonic stem cells for cardiomyogenesis." Journal of Molecular and Cellular Cardiology 45, no. 4 (October 2008): 462–74. http://dx.doi.org/10.1016/j.yjmcc.2008.08.008.

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8

Ali, Enas Hussein, Fatemeh Sharifpanah, Amer Taha, Suk Ying Tsang, Maria Wartenberg, and Heinrich Sauer. "The Milk Thistle (Silybum marianum) Compound Silibinin Inhibits Cardiomyogenesis of Embryonic Stem Cells by Interfering with Angiotensin II Signaling." Stem Cells International 2018 (December 13, 2018): 1–10. http://dx.doi.org/10.1155/2018/9215792.

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The milk thistle (Silybum marianum (L.) Gaertn.) compound silibinin may be an inhibitor of the angiotensin II type 1 (AT1) receptor which is expressed in differentiating embryonic stem (ES) cells and is involved in the regulation of cardiomyogenesis. In the present study, it was demonstrated that silibinin treatment decreased the number of spontaneously contracting cardiac foci and cardiac cell areas differentiated from ES cells as well as contraction frequency and frequency of calcium (Ca2+) spiking. In contrast, angiotensin II (Ang II) treatment stimulated cardiomyogenesis as well as contraction and Ca2+ spiking frequency, which were abolished in the presence of silibinin. Intracellular Ca2+ transients elicited by Ang II in rat smooth muscle cells were not impaired upon silibinin treatment, excluding the possibility that the compound acted on the AT1 receptor. Ang II treatment activated extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun NH2-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) pathways in embryoid bodies which were abolished upon silibinin pretreatment. In summary, our data suggest that silibinin inhibits cardiomyogenesis of ES cells by interfering with Ang II signaling downstream of the AT1 receptor.

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9

Humpolíček, P., K. A. Radaszkiewicz, V. Kašpárková, J. Stejskal, M. Trchová, Z. Kuceková, H. Vičarová, J. Pacherník, M. Lehocký, and A. Minařík. "Stem cell differentiation on conducting polyaniline." RSC Advances 5, no. 84 (2015): 68796–805. http://dx.doi.org/10.1039/c5ra12218j.

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10

Mobley, Stephen, Jessica M. Shookhof, Kara Foshay, Michelle Park, and G. Ian Gallicano. "PKG and PKC Are Down-Regulated during Cardiomyocyte Differentiation from Embryonic Stem Cells: Manipulation of These Pathways Enhances Cardiomyocyte Production." Stem Cells International 2010 (2010): 1–10. http://dx.doi.org/10.4061/2010/701212.

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Understanding signal transduction mechanisms that drive differentiation of adult or embryonic stem cells (ESCs) is imperative if they are to be used to cure disease. While the list of signaling pathways regulating stem cell differentiation is growing, it is far from complete. Indentifying regulatory mechanisms and timecourse commitment to cell lineages is needed for generating pure populations terminally differentiated cell types, and in ESCs, suppression of teratoma formation. To this end, we investigated specific signaling mechanisms involved in cardiomyogenesis, followed by manipulation of these pathways to enhance differentiation of ESCs into cardiomyocytes. Subjecting nascent ESC-derived cardiomyocytes to a proteomics assay, we found that cardiomyogenesis is influenced by up- and down-regulation of a number of kinases, one of which, cGMP-dependent protein kinase (PKG), is markedly down-regulated during differentiation. Delving further, we found that manipulating the PKG pathway using PKG-specific inhibitors produced significantly more cardiomyocytes from ESCs when compared to ESCs left to differentiate without inhibitors. In addition, we found combinatorial effects when culturing ESCs in inhibitors to PKG and PKC isotypes. Consequently, we have generated a novel hypothesis: Down-regulation of PKG and specific PKC pathways are necessary for cardiomyogenesis, and when manipulated, these pathways produce significantly more cardiomyocytes than untreated ESCs.

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11

Aguilar, Jose S., Aynun N. Begum, Jonathan Alvarez, Xiao-bing Zhang, Yiling Hong, and Jijun Hao. "Directed cardiomyogenesis of human pluripotent stem cells by modulating Wnt/β-catenin and BMP signalling with small molecules." Biochemical Journal 469, no. 2 (July 6, 2015): 235–41. http://dx.doi.org/10.1042/bj20150186.

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12

Danalache, Bogdan A., Joanne Paquin, Wang Donghao, Ryszard Grygorczyk, Jennifer C. Moore, Christine L. Mummery, Jolanta Gutkowska, and Marek Jankowski. "Nitric Oxide Signaling in Oxytocin-Mediated Cardiomyogenesis." STEM CELLS 25, no. 3 (November 30, 2006): 679–88. http://dx.doi.org/10.1634/stemcells.2005-0610.

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13

Jamali, Mina, Parker J. Rogerson, Sharon Wilton, and Ilona S. Skerjanc. "Nkx2–5 Activity Is Essential for Cardiomyogenesis." Journal of Biological Chemistry 276, no. 45 (August 28, 2001): 42252–58. http://dx.doi.org/10.1074/jbc.m107814200.

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14

Traister, Alexandra, Shabana Aafaqi, Stephane Masse, Xiaojing Dai, Mark Li, Aleksander Hinek, Kumaraswamy Nanthakumar, Gregory Hannigan, and John G. Coles. "ILK Induces Cardiomyogenesis in the Human Heart." PLoS ONE 7, no. 5 (May 29, 2012): e37802. http://dx.doi.org/10.1371/journal.pone.0037802.

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15

Gianakopoulos, Peter J., and Ilona S. Skerjanc. "Hedgehog Signaling Induces Cardiomyogenesis in P19 Cells." Journal of Biological Chemistry 280, no. 22 (March 26, 2005): 21022–28. http://dx.doi.org/10.1074/jbc.m502977200.

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16

Kami, Daisuke, Ichiro Shiojima, Hatsune Makino, Kenji Matsumoto, Yoriko Takahashi, Ryuga Ishii, Atsuhiko T. Naito, et al. "Gremlin Enhances the Determined Path to Cardiomyogenesis." PLoS ONE 3, no. 6 (June 11, 2008): e2407. http://dx.doi.org/10.1371/journal.pone.0002407.

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17

Pereira, Isabela Tiemy, Lucia Spangenberg, Guillermo Cabrera, and Bruno Dallagiovanna. "Polysome-associated lncRNAs during cardiomyogenesis of hESCs." Molecular and Cellular Biochemistry 468, no. 1-2 (March 3, 2020): 35–45. http://dx.doi.org/10.1007/s11010-020-03709-7.

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18

Yilbas, Ayse Elif, Hymn Mach, and Qiao Li. "The role of histone acetyltransferases in cardiomyogenesis." Current Opinion in Biotechnology 22 (September 2011): S50. http://dx.doi.org/10.1016/j.copbio.2011.05.132.

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19

Hrabchak, Christopher, Maurice Ringuette, and Kimberly Woodhouse. "Recombinant mouse SPARC promotes parietal endoderm differentiation and cardiomyogenesis in embryoid bodies." Biochemistry and Cell Biology 86, no. 6 (December 2008): 487–99. http://dx.doi.org/10.1139/o08-141.

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In the absence of leukemia inhibitory factor, murine embryonic stem cells cultured in vitro spontaneously aggregate to from three-dimensional embryoid bodies that differentiate to produce hematopoietic, endothelial, muscle, and neuronal cell lineages in a manner recapitulating the events of early embryogenesis. Cardiomyogenesis in embryoid bodies was recently demonstrated to be promoted by PYS-2-derived native SPARC (secreted protein, acidic and rich in cysteine), whose expression is upregulated in parietal endoderm at the onset of the epithelial to mesenchymal transition. Here, we confirm the stimulatory effects of mouse SPARC on cardiomyogenesis using a recombinant baculovirus-produced protein (rmSPARC). Embryoid bodies cultured in the presence of glycosylated rmSPARC, or an unglycosylated peptide spanning the C-terminal EF-hand domain, developed greater numbers of beating cardiomyocytes than did time-matched controls, with enhanced expression of cardiac marker genes including Nkx2.5, Troponin, BMP-2, and MHCα. Histochemical analysis revealed an expansion of the peripheral endoderm, with thicker layers of extracellular matrix (ECM) material observed atop underlying cells. Embryoid bodies treated with SPARC also displayed increased adherence to polystyrene culture dishes, with enhanced expression of ECM mRNAs including collagen IVα3, collagen IVα5, and laminin α1. These results indicate that, in addition to the promotion of cardiomyogenesis, SPARC may also help regulate the molecular composition and organization of ECM secreted by the mesenchymal parietal endoderm.

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20

Gutkowska, J., B. A. Danalache, M. Jankowski, and J. Paquin. "ROLE OF NITRIC OXIDE IN OXYTOCIN-INDUCED CARDIOMYOGENESIS." Journal of Hypertension 22, Suppl. 2 (June 2004): S175—S176. http://dx.doi.org/10.1097/00004872-200406002-00604.

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21

Happe, Cassandra L., and Adam J. Engler. "Mechanical Forces Reshape Differentiation Cues That Guide Cardiomyogenesis." Circulation Research 118, no. 2 (January 22, 2016): 296–310. http://dx.doi.org/10.1161/circresaha.115.305139.

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22

Hosoda, T., D. D'Amario, M. C. Cabral-Da-Silva, H. Zheng, M. E. Padin-Iruegas, B. Ogorek, J. Ferreira-Martins, et al. "Clonality of mouse and human cardiomyogenesis in vivo." Proceedings of the National Academy of Sciences 106, no. 40 (September 17, 2009): 17169–74. http://dx.doi.org/10.1073/pnas.0903089106.

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23

Karamboulas, C., G. D. Dakubo, J. Liu, Y. De Repentigny, K. Yutzey, V. A. Wallace, R. Kothary, and I. S. Skerjanc. "Disruption of MEF2 activity in cardiomyoblasts inhibits cardiomyogenesis." Journal of Cell Science 119, no. 20 (October 15, 2006): 4315–21. http://dx.doi.org/10.1242/jcs.03186.

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24

Karamboulas, C., G. D. Dakubo, J. Liu, Y. De Repentigny, K. Yutzey, V. A. Wallace, R. Kothary, and I. S. Skerjanc. "Disruption of MEF2 activity in cardiomyoblasts inhibits cardiomyogenesis." Journal of Cell Science 120, no. 1 (December 12, 2006): 200. http://dx.doi.org/10.1242/jcs.03369.

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25

Karamboulas, C., G. D. Dakubo, J. Liu, Y. De Repentigny, K. Yutzey, V. A. Wallace, R. Kothary, and I. S. Skerjanc. "Disruption of MEF2 activity in cardiomyoblasts inhibits cardiomyogenesis." Journal of Cell Science 119, no. 20 (October 15, 2006): 4367. http://dx.doi.org/10.1242/jcs.03370.

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26

Bloch, W. "Nitric oxide synthase expression and role during cardiomyogenesis." Cardiovascular Research 43, no. 3 (August 15, 1999): 675–84. http://dx.doi.org/10.1016/s0008-6363(99)00160-1.

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27

Kajstura, Jan, Marcello Rota, Donato Cappetta, Barbara Ogórek, Christian Arranto, Yingnan Bai, João Ferreira-Martins, et al. "Cardiomyogenesis in the Aging and Failing Human Heart." Circulation 126, no. 15 (October 9, 2012): 1869–81. http://dx.doi.org/10.1161/circulationaha.112.118380.

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28

Wang, Bingyan, Alvin Muliono, Roberto Alvarez, and Mark Sussman. "Cardiac Progenitor Cell Lineage Tracing During Embryonic Cardiomyogenesis." Journal of Molecular and Cellular Cardiology 112 (November 2017): 138. http://dx.doi.org/10.1016/j.yjmcc.2017.07.027.

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29

Jamali, Mina, Christina Karamboulas, Parker J. Rogerson, and Ilona S. Skerjanc. "BMP signaling regulates Nkx2-5 activity during cardiomyogenesis." FEBS Letters 509, no. 1 (November 27, 2001): 126–30. http://dx.doi.org/10.1016/s0014-5793(01)03151-9.

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30

Sato, Mariko, and H. Joseph Yost. "Cardiac neural crest contributes to cardiomyogenesis in zebrafish." Developmental Biology 257, no. 1 (May 2003): 127–39. http://dx.doi.org/10.1016/s0012-1606(03)00037-x.

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31

Berkessel, Albrecht, Bianca Seelig, Silke Schwengberg, Jürgen Hescheler, and Agapios Sachinidis. "Chemically Induced Cardiomyogenesis of Mouse Embryonic Stem Cells." ChemBioChem 11, no. 2 (December 28, 2009): 208–17. http://dx.doi.org/10.1002/cbic.200900345.

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32

Karra, Ravi, Matthew J. Foglia, Wen-Yee Choi, Christine Belliveau, Paige DeBenedittis, and Kenneth D. Poss. "Vegfaa instructs cardiac muscle hyperplasia in adult zebrafish." Proceedings of the National Academy of Sciences 115, no. 35 (August 13, 2018): 8805–10. http://dx.doi.org/10.1073/pnas.1722594115.

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During heart development and regeneration, coronary vascularization is tightly coupled with cardiac growth. Although inhibiting vascularization causes defects in the innate regenerative response of zebrafish to heart injury, angiogenic signals are not known to be sufficient for triggering regeneration events. Here, by using a transgenic reporter strain, we found that regulatory sequences of the angiogenic factor vegfaa are active in epicardial cells of uninjured animals, as well as in epicardial and endocardial tissue adjacent to regenerating muscle upon injury. Additionally, we find that induced cardiac overexpression of vegfaa in zebrafish results in overt hyperplastic thickening of the myocardial wall, accompanied by indicators of angiogenesis, epithelial-to-mesenchymal transition, and cardiomyocyte regeneration programs. Unexpectedly, vegfaa overexpression in the context of cardiac injury enabled ectopic cardiomyogenesis but inhibited regeneration at the site of the injury. Our findings identify Vegfa as one of a select few known factors sufficient to activate adult cardiomyogenesis, while also illustrating how instructive factors for heart regeneration require spatiotemporal control for efficacy.

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Parisi, Silvia, Daniela D'Andrea, Carmine T. Lago, Eileen D. Adamson, M. Graziella Persico, and Gabriella Minchiotti. "Nodal-dependent Cripto signaling promotes cardiomyogenesis and redirects the neural fate of embryonic stem cells." Journal of Cell Biology 163, no. 2 (October 27, 2003): 303–14. http://dx.doi.org/10.1083/jcb.200303010.

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The molecular mechanisms controlling inductive events leading to the specification and terminal differentiation of cardiomyocytes are still largely unknown. We have investigated the role of Cripto, an EGF-CFC factor, in the earliest stages of cardiomyogenesis. We find that both the timing of initiation and the duration of Cripto signaling are crucial for priming differentiation of embryonic stem (ES) cells into cardiomyocytes, indicating that Cripto acts early to determine the cardiac fate. Furthermore, we show that failure to activate Cripto signaling in this early window of time results in a direct conversion of ES cells into a neural fate. Moreover, the induction of Cripto activates the Smad2 pathway, and overexpression of activated forms of type I receptor ActRIB compensates for the lack of Cripto signaling in promoting cardiomyogenesis. Finally, we show that Nodal antagonists inhibit Cripto-regulated cardiomyocyte induction and differentiation in ES cells. All together our findings provide evidence for a novel role of the Nodal/Cripto/Alk4 pathway in this process.

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34

Chen, Yanmei, Chuanxi Zhang, Shuxin Shen, Shengcun Guo, Lintao Zhong, Xinzhong Li, Guojun Chen, et al. "Ultrasound-targeted microbubble destruction enhances delayed BMC delivery and attenuates post-infarction cardiac remodelling by inducing engraftment signals." Clinical Science 130, no. 23 (October 20, 2016): 2105–20. http://dx.doi.org/10.1042/cs20160085.

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Appropriate ultrasound-targeted microbubble destruction (UTMD) treatment enhanced engraftment signals at 14 days post-ischaemia/reperfusion (post-I/R). Delayed bone marrow cell (BMC) transplantation combined with UTMD treatment attenuated post-infarction cardiac remodelling. Delayed BMC transplantation combined with UTMD treatment promoted angiogenesis, cardiomyogenesis and expansion of cardiac c-kit+ cells.

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35

Maes, Olivier. "Proteomics of RNA polymerase II holoenzymes during P19 cardiomyogenesis." Open Life Sciences 2, no. 4 (December 1, 2007): 518–37. http://dx.doi.org/10.2478/s11535-007-0040-z.

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AbstractThe embryonal carcinoma P19 model has allowed the elucidation of a role for several transcription factors in cell differentiation. Here, the regulation of the RNA polymerase II machinery has been explored through its association with multifunctional complexes involved in transcription. An interaction proteomics analysis of TFIIS-purified RNA polymerase II (RNAPII) holoenzymes during cardiomyogenesis is described. Modifications of protein complexes that may be associated with transcriptionally active and activator responsive RNAPII holoenzymes were detected in a serum and DMSO dependent manner. Subunits of the PAF1 and Mediator complexes were correlated with holoenzymes from non-differentiated and terminally differentiated P19 cultures respectively. Moreover, high levels of nucleolin were identified in all forms of holoenzymes by two-dimensional gel electrophoresis, and suggest that nucleolin could bind to RNAPII and TFIIS. Several proteins that were identified in the RNAPII holoenzymes are known to have functions in mRNA processing and may bind to nucleolin. A novel function for nucleolin is proposed as a possible pivotal platform between transcription, mRNA processing and export.

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Wu, Xu, Sheng Ding, Qiang Ding, Nathanael S. Gray, and Peter G. Schultz. "Small Molecules that Induce Cardiomyogenesis in Embryonic Stem Cells." Journal of the American Chemical Society 126, no. 6 (February 2004): 1590–91. http://dx.doi.org/10.1021/ja038950i.

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37

Zheng, Bin, Jin-Kun Wen, and Mei Han. "hhLIM is involved in cardiomyogenesis of embryonic stem cells." Biochemistry (Moscow) 71, S1 (January 2006): S71—S76. http://dx.doi.org/10.1134/s0006297906130128.

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38

Stary, Martina, Waltraud Pasteiner, Alexandra Summer, Astrid Hrdina, Andreas Eger, and Georg Weitzer. "Parietal endoderm secreted SPARC promotes early cardiomyogenesis in vitro." Experimental Cell Research 310, no. 2 (November 2005): 331–43. http://dx.doi.org/10.1016/j.yexcr.2005.07.013.

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39

Kanno, S., P. K. M. Kim, K. Sallam, J. Lei, T. R. Billiar, and L. L. Shears. "Nitric oxide facilitates cardiomyogenesis in mouse embryonic stem cells." Proceedings of the National Academy of Sciences 101, no. 33 (August 10, 2004): 12277–81. http://dx.doi.org/10.1073/pnas.0401557101.

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Mohri, Tomomi, Tomohiko Iwakura, Hiroyuki Nakayama, and Yasushi Fujio. "JAK-STAT signaling in cardiomyogenesis of cardiac stem cells." JAK-STAT 1, no. 2 (April 2012): 125–30. http://dx.doi.org/10.4161/jkst.20296.

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Adam Young, D., Jessica A. DeQuach, and Karen L. Christman. "Human cardiomyogenesis and the need for systems biology analysis." Wiley Interdisciplinary Reviews: Systems Biology and Medicine 3, no. 6 (December 31, 2010): 666–80. http://dx.doi.org/10.1002/wsbm.141.

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Van Handel, Ben, Amélie Montel-Hagen, Rajkumar Sasidharan, Haruko Nakano, Roberto Ferrari, Cornelis J. Boogerd, Johann Schredelseker, et al. "Scl Represses Cardiomyogenesis in Prospective Hemogenic Endothelium and Endocardium." Cell 150, no. 3 (August 2012): 590–605. http://dx.doi.org/10.1016/j.cell.2012.06.026.

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Verjans, Robin, Marc van Bilsen, and Blanche Schroen. "Reviewing the Limitations of Adult Mammalian Cardiac Regeneration: Noncoding RNAs as Regulators of Cardiomyogenesis." Biomolecules 10, no. 2 (February 10, 2020): 262. http://dx.doi.org/10.3390/biom10020262.

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Abstract:

The adult mammalian heart is incapable of regeneration following cardiac injury, leading to a decline in function and eventually heart failure. One of the most evident barriers limiting cardiac regeneration is the inability of cardiomyocytes to divide. It has recently become clear that the mammalian heart undergoes limited cardiomyocyte self-renewal throughout life and is even capable of modest regeneration early after birth. These exciting findings have awakened the goal to promote cardiomyogenesis of the human heart to repair cardiac injury or treat heart failure. We are still far from understanding why adult mammalian cardiomyocytes possess only a limited capacity to proliferate. Identifying the key regulators may help to progress towards such revolutionary therapy. Specific noncoding RNAs control cardiomyocyte division, including well explored microRNAs and more recently emerged long noncoding RNAs. Elucidating their function and molecular mechanisms during cardiomyogenesis is a prerequisite to advance towards therapeutic options for cardiac regeneration. In this review, we present an overview of the molecular basis of cardiac regeneration and describe current evidence implicating microRNAs and long noncoding RNAs in this process. Current limitations and future opportunities regarding how these regulatory mechanisms can be harnessed to study myocardial regeneration will be addressed.

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Nemade, Harshal, Aviseka Acharya, Umesh Chaudhari, Erastus Nembo, Filomain Nguemo, Nicole Riet, Hinrich Abken, Jürgen Hescheler, Symeon Papadopoulos, and Agapios Sachinidis. "Cyclooxygenases Inhibitors Efficiently Induce Cardiomyogenesis in Human Pluripotent Stem Cells." Cells 9, no. 3 (February 27, 2020): 554. http://dx.doi.org/10.3390/cells9030554.

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Abstract:

Application of human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) is limited by the challenges in their efficient differentiation. Recently, the Wingless (Wnt) signaling pathway has emerged as the key regulator of cardiomyogenesis. In this study, we evaluated the effects of cyclooxygenase inhibitors on cardiac differentiation of hPSCs. Cardiac differentiation was performed by adherent monolayer based method using 4 hPSC lines (HES3, H9, IMR90, and ES4SKIN). The efficiency of cardiac differentiation was evaluated by flow cytometry and RT-qPCR. Generated hPSC-CMs were characterised using immunocytochemistry, electrophysiology, electron microscopy, and calcium transient measurements. Our data show that the COX inhibitors Sulindac and Diclofenac in combination with CHIR99021 (GSK-3 inhibitor) efficiently induce cardiac differentiation of hPSCs. In addition, inhibition of COX using siRNAs targeted towards COX-1 and/or COX-2 showed that inhibition of COX-2 alone or COX-1 and COX-2 in combination induce cardiomyogenesis in hPSCs within 12 days. Using IMR90-Wnt reporter line, we showed that inhibition of COX-2 led to downregulation of Wnt signalling activity in hPSCs. In conclusion, this study demonstrates that COX inhibition efficiently induced cardiogenesis via modulation of COX and Wnt pathway and the generated cardiomyocytes express cardiac-specific structural markers as well as exhibit typical calcium transients and action potentials. These cardiomyocytes also responded to cardiotoxicants and can be relevant as an in vitro cardiotoxicity screening model.

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Kitamura, Ryoji, Tomosaburo Takahashi, Norio Nakajima, Koji Isodono, Satoshi Asada, Tomomi Ueyama, Hiroaki Matsubara, and Hidemasa Oh. "Activation of endogenous Smad2 modulates cardiomyogenesis in embryonic stem cells." Journal of Molecular and Cellular Cardiology 44, no. 2 (February 2008): 447. http://dx.doi.org/10.1016/j.yjmcc.2007.07.038.

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Kim, B., S. W. Oh, M. N. Lee, J. R. Ha, H. J. Jeon, S. K. Son, M. R. Lee, et al. "SMALL MOLECULES THAT PROMOTE CARDIOMYOGENESIS IN MOUSE EMBRYONIC STEM CELLS." Atherosclerosis Supplements 9, no. 1 (May 2008): 59. http://dx.doi.org/10.1016/s1567-5688(08)70234-4.

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Stary, Martina, Mikael Schneider, Søren P. Sheikh, and Georg Weitzer. "Parietal endoderm secreted S100A4 promotes early cardiomyogenesis in embryoid bodies." Biochemical and Biophysical Research Communications 343, no. 2 (May 2006): 555–63. http://dx.doi.org/10.1016/j.bbrc.2006.02.161.

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Parveen, Shagufta, Shishu Pal Singh, M. M. Panicker, and Pawan Kumar Gupta. "Amniotic membrane as novel scaffold for human iPSC-derived cardiomyogenesis." In Vitro Cellular & Developmental Biology - Animal 55, no. 4 (February 24, 2019): 272–84. http://dx.doi.org/10.1007/s11626-019-00321-y.

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Martin, Jennifer, Boni A. Afouda, and Stefan Hoppler. "Wnt/β-catenin signalling regulates cardiomyogenesis via GATA transcription factors." Journal of Anatomy 216, no. 1 (January 2010): 92–107. http://dx.doi.org/10.1111/j.1469-7580.2009.01171.x.

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Horton, Renita E., and Debra T. Auguste. "Synergistic effects of hypoxia and extracellular matrix cues in cardiomyogenesis." Biomaterials 33, no. 27 (September 2012): 6313–19. http://dx.doi.org/10.1016/j.biomaterials.2012.05.063.

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