scholarly journals Chemicals Regulating Cardiomyocyte Differentiation

10.5772/15489 ◽  
2011 ◽  
Author(s):  
Hideki Uosaki ◽  
Jun K
Keyword(s):  
Cardiomyocyte Differentiation

Genetic ablation of monoamine oxidases impairs cardiomyocyte differentiation from hiPSc

2018 ◽  
Vol 120 ◽  
pp. 3
Author(s):  
M. Di Sante ◽  
E. Greotti ◽  
S. Antonucci ◽  
F. Mazza ◽  
C. Troiano ◽  
...  
Keyword(s):  
Cardiomyocyte Differentiation ◽  
Monoamine Oxidases ◽  
Genetic Ablation

scholarly journals Pten Regulates Cardiomyocyte Differentiation by Modulating Non‐CG Methylation via Dnmt3 (Adv. Sci. 17/2021)

2021 ◽  
Vol 8 (17) ◽  
pp. 2170107
Author(s):  
Wuming Wang ◽  
Gang Lu ◽  
Hong‐Bin Liu ◽  
Zhiqiang Xiong ◽  
Ho‐Duen Leung ◽  
...  
Keyword(s):  
Cardiomyocyte Differentiation

Abstract P412: Mitochondrial Metabolic Transcriptome Profiles During Cardiomyocyte Differentiation From Mouse And Human Pluripotent Stem Cells

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Sung Woo Cho ◽  
Hyoung Kyu Kim ◽  
Jin Han ◽  
Ji-Hee Sung
Keyword(s):  
Stem Cells ◽  
Pluripotent Stem Cells ◽  
Oxidative Metabolism ◽  
Time Dependent ◽  
Lineage Commitment ◽  
Simultaneous Increase ◽  
Dependent Manner ◽  
Cardiomyocyte Differentiation ◽  
Cardiac Lineage ◽  
Mitochondrial Oxidative Metabolism

Simultaneous increase of myofibrils and mitochondria is a key process of cardiomyocyte differentiation from pluripotent stem cells (PSCs). Specifically, development of mitochondrial oxidative energy metabolism in cardiomyocytes is essential to providing the beating function. Although previous studies reported that mitochondrial oxidative metabolism have some correlation with the differentiation of cardiomyocytes, the mechanism by which mitochondrial oxidative metabolism is regulated and the link between cardiomyogenesis and mitochondrial function are still poorly understood. In the present study, we performed transcriptome analysis on cells at specific stages of cardiomyocyte differentiation from mouse embryonic stem cells (mESCs) and human induced PSCs (hiPSCs). We selected highly upregulated mitochondrial metabolic genes at cardiac lineage commitment and time-dependent manner during cardiomyocyte differentiation and identified the protein-protein interaction network connecting between mitochondrial metabolic and cardiac developmental genes. We found several mitochondrial metabolic regulatory genes at cardiac lineage commitment (Cck, Bdnf, Fabp4, Cebpa, Cdkn2a in mESC-derived cells and CCK, NOS3 in hiPSC-derived cells) and time-dependent manner during cardiomyocyte differentiation (Eno3, Pgam2, Cox6a2, Fabp3 in mESC-derived cells and PGAM2, SLC25A4 in hiPSC-derived cells). Notably, mitochondrial metabolic proteins are highly interacted with cardiac developmental proteins time-dependent manner during cardiomyocyte differentiation rather than cardiac lineage commitment. Furthermore, mitochondrial metabolic proteins are mainly interacted with cardiac muscle contractile proteins rather than cardiac transcription factors in cardiomyocyte. Therefore, mitochondrial metabolism is critical at cardiac maturation rather than cardiac lineage commitment.

scholarly journals Deacetylation of Histone H4 Accompanying Cardiomyogenesis is Weakened in HDAC1-Depleted ES Cells

2018 ◽  
Vol 19 (8) ◽  
pp. 2425 ◽  
Author(s):  
Orazio Angelo Arcidiacono ◽  
Jana Krejčí ◽  
Jana Suchánková ◽  
Eva Bártová
Keyword(s):  
Histone Deacetylases ◽  
Trichostatin A ◽  
Es Cells ◽  
Embryonic Stem ◽  
Cardiomyocyte Differentiation ◽  
Histone H4 ◽  
Epigenetic Factors ◽  
Double Knockout ◽  
Physiological Processes

Cell differentiation into cardiomyocytes requires activation of differentiation-specific genes and epigenetic factors that contribute to these physiological processes. This study is focused on the in vitro differentiation of mouse embryonic stem cells (mESCs) induced into cardiomyocytes. The effects of clinically promising inhibitors of histone deacetylases (HDACi) on mESC cardiomyogenesis and on explanted embryonic hearts were also analyzed. HDAC1 depletion caused early beating of cardiomyocytes compared with those of the wild-type (wt) counterpart. Moreover, the adherence of embryonic bodies (EBs) was reduced in HDAC1 double knockout (dn) mESCs. The most important finding was differentiation-specific H4 deacetylation observed during cardiomyocyte differentiation of wt mESCs, while H4 deacetylation was weakened in HDAC1-depleted cells induced to the cardiac pathway. Analysis of the effect of HDACi showed that Trichostatin A (TSA) is a strong hyperacetylating agent, especially in wt mESCs, but only SAHA reduced the size of the beating areas in EBs that originated from HDAC1 dn mESCs. Additionally, explanted embryonic hearts (e15) responded to treatment with HDACi: all of the tested HDACi (TSA, SAHA, VPA) increased the levels of H3K9ac, H4ac, H4K20ac, and pan-acetylated lysines in embryonic hearts. This observation shows that explanted tissue can be maintained in a hyperacetylation state several hours after excision, which appears to be useful information from the view of transplantation strategy and the maintenance of gene upregulation via acetylation in tissue intended for transplantation.

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