scholarly journals Anterior endoderm is a specific effector of terminal cardiac myocyte differentiation of cells from the embryonic heart forming region

1994 ◽  
Vol 200 (2) ◽  
pp. 155-162 ◽  
Author(s):  
Yukiko Sugi ◽  
John Lough
Keyword(s):  
Cardiac Myocyte ◽  
Embryonic Heart ◽  
Specific Effector ◽  
Myocyte Differentiation

scholarly journals MicroRNA-1 transfected embryonic stem cells enhance cardiac myocyte differentiation and inhibit apoptosis by modulating the PTEN/Akt pathway in the infarcted heart

2011 ◽  
Vol 301 (5) ◽  
pp. H2038-H2049 ◽  
Author(s):  
Carley Glass ◽  
Dinender K. Singla
Keyword(s):  
Cell Differentiation ◽  
Cardiac Myocyte ◽  
Heart Function ◽  
Es Cells ◽  
Embryonic Stem ◽  
Stem Cell Differentiation ◽  
Border Zone ◽  
Es Cell ◽  
Infarcted Heart ◽  
Myocyte Differentiation

microRNAs (miRs) have emerged as critical modulators of various physiological processes including stem cell differentiation. Indeed, miR-1 has been reported to play an integral role in the regulation of cardiac muscle progenitor cell differentiation. However, whether overexpression of miR-1 in embryonic stem (ES) cells (miR-1-ES cells) will enhance cardiac myocyte differentiation following transplantation into the infarcted myocardium is unknown. In the present study, myocardial infarction (MI) was produced in C57BL/6 mice by left anterior descending artery ligation. miR-1-ES cells, ES cells, or culture medium (control) was transplanted into the border zone of the infarcted heart, and 2 wk post-MI, cardiac myocyte differentiation, adverse ventricular remodeling, and cardiac function were assessed. We provide evidence demonstrating enhanced cardiac myocyte commitment of transplanted miR-1-ES cells in the mouse infarcted heart as compared with ES cells. Assessment of apoptosis revealed that overexpression of miR-1 in transplanted ES cells protected host myocardium from MI-induced apoptosis through activation of p-AKT and inhibition of caspase-3, phosphatase and tensin homolog, and superoxide production. A significant reduction in interstitial and vascular fibrosis was quantified in miR-1-ES cell and ES cell transplanted groups compared with control MI. However, no statistical significance between miR-1-ES cell and ES cell groups was observed. Finally, mice receiving miR-1-ES cell transplantation post-MI had significantly improved heart function compared with respective controls ( P < 0.05). Our data suggest miR-1 drives cardiac myocyte differentiation from transplanted ES cells and inhibits apoptosis post-MI, ultimately giving rise to enhanced cardiac repair, regeneration, and function.

scholarly journals Pharmacological priming of adipose-derived stem cells promotes myocardial repair

2016 ◽  
Vol 64 (1) ◽  
pp. 50-62 ◽  
Author(s):  
Jana S Burchfield ◽  
Ashley L Paul ◽  
Vishy Lanka ◽  
Wei Tan ◽  
Yongli Kong ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cardiac Function ◽  
Functional Recovery ◽  
Cardiac Myocyte ◽  
Left Ventricular ◽  
Adipose Derived Stem Cells ◽  
Myocardial Repair ◽  
Myocyte Differentiation

Adipose-derived stem cells (ADSCs) have myocardial regeneration potential, and transplantation of these cells following myocardial infarction (MI) in animal models leads to modest improvements in cardiac function. We hypothesized that pharmacological priming of pre-transplanted ADSCs would further improve left ventricular functional recovery after MI. We previously identified a compound from a family of 3,5-disubstituted isoxazoles, ISX1, capable of activating an Nkx2-5-driven promoter construct. Here, using ADSCs, we found that ISX1 (20 mM, 4 days) triggered a robust, dose-dependent, fourfold increase in Nkx2-5 expression, an early marker of cardiac myocyte differentiation and increased ADSC viability in vitro. Co-culturing neonatal cardiomyocytes with ISX1-treated ADSCs increased early and late cardiac gene expression. Whereas ISX1 promoted ADSC differentiation toward a cardiogenic lineage, it did not elicit their complete differentiation or their differentiation into mature adipocytes, osteoblasts, or chondrocytes, suggesting that re-programming is cardiomyocyte specific. Cardiac transplantation of ADSCs improved left ventricular functional recovery following MI, a response which was significantly augmented by transplantation of ISX1- pretreated cells. Moreover, ISX1-treated and transplanted ADSCs engrafted and were detectable in the myocardium 3 weeks following MI, albeit at relatively small numbers. ISX1 treatment increased histone acetyltransferase (HAT) activity in ADSCs, which was associated with histone 3 and histone 4 acetylation. Finally, hearts transplanted with ISX1-treated ADSCs manifested significant increases in neovascularization, which may account for the improved cardiac function. These findings suggest that a strategy of drug-facilitated initiation of myocyte differentiation enhances exogenously transplanted ADSC persistence in vivo, and consequent tissue neovascularization, to improve cardiac function.

Cardiac myocyte differentiation: the Nkx2.5 and Cripto target genes in P19 clone 6 cells

2005 ◽  
Vol 5 (4) ◽  
pp. 218-239 ◽  
Author(s):  
Hailing Liu ◽  
Thomas M. Harris ◽  
Hyung H. Kim ◽  
Geoffrey Childs
Keyword(s):  
Target Genes ◽  
Cardiac Myocyte ◽  
Myocyte Differentiation

Abstract P092: Simplified Monolayer Differentiation of Human-Induced Pluripotent Stem Cells to Functional Cardiac Myocytes

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Jennifer K Lang ◽  
Stanley Fernandez ◽  
Thomas Cimato
Keyword(s):  
Stem Cells ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cardiac Myocytes ◽  
Pluripotent Stem Cells ◽  
Action Potentials ◽  
Cardiac Myocyte ◽  
Human Ipscs ◽  
Myocyte Differentiation ◽  
Induced Pluripotent

Background: Human induced pluripotent stem cells (hiPSCs) are an important model for cardiovascular research, drug discovery, and translational research applications. Commonly used methods to direct iPSCs to cardiac myocytes can be technically demanding. Prior studies have shown that both VEGF and endothelial cells promote differentiation of stem cells to cardiac myocytes. Furthermore, DMEM/F12 with 10% fetal calf serum (DMEM-FCS) has been shown to induce cardiac myocytes in an embryoid body (EB) system. The objective of this study was to determine if differentiation of hiPSCs using conditions that support endothelial cell differentiation would promote cardiac myocyte colony formation. Methods: Two hiPSC lines derived using non-genome integrating methods were maintained on Matrigel-coated surfaces under serum free conditions in mTeSR1 medium. We performed a comparison of monolayer myocyte differentiation efficiency using DMEM-FCS and endothelial cell medium (EC). Cells were maintained in iPSC medium (mTeSR1) as a negative control. The number of beating colonies derived under each growth condition was determined using phase microscopy at 4 weeks. Cardiac myocyte commitment was characterized using an α-MHC-GFP reporter vector and electrophysiologic action potentials on isolated beating colonies. Results: Differentiation of human iPSCs in EC medium induced substantial numbers of beating colonies 4 weeks after differentiation (2.29 ± 0.3 beating colonies/cm2 culture area, n=42). Unlike EB models of myocyte differentiation, no beating clusters were observed in our monolayer system with DMEM-FCS medium (n=14) (p<0.01). As expected, mTESR1 (n=12) did not induce any cardiac myocytes. All beating cell colonies expressed GFP driven by the cardiac specific α-MHC promoter. Electrophysiological studies confirmed the presence of action potentials with ventricular phenotypes. Conclusions: Differentiation of human iPSCs under monolayer conditions that support endothelial cells facilitates efficient induction of functional human cardiac myocytes. Our findings simplify the differentiation of iPSCs to cardiac myocytes, making research with human iPSCs more accessible to a broad range of cardiovascular investigators.

Identification of a novel cardiac-specific transcript critical for cardiac myocyte differentiation

Development ◽  
1996 ◽  
Vol 122 (9) ◽  
pp. 2779-2789 ◽  
Author(s):  
Y. Wei ◽  
D. Bader ◽  
J. Litvin
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Cardiac Myocyte ◽  
Heart Tube ◽  
Myogenic Cells ◽  
Chicken Heart ◽  
Reading Frame ◽  
Cardiac Myogenesis ◽  
Myocyte Differentiation ◽  
Heart Formation

A novel cDNA, pCMF1, which is expressed exclusively and transiently in the myogenic cells of the differentiating chicken heart was isolated and characterized. The full-length cDNA of pCMF1 has one open reading frame encoding 1538 predicted amino acids. While computer analysis predicts the presence of specific structural motifs, the overall sequence of pCMF1 is unique. The pattern of pCMF1 gene expression during heart formation was determined by whole-mount in situ hybridization. pCMF1 is transiently expressed within the myogenic cells of the primitive heart tube from stages 9 to 18 and is not detected in the heart or any other tissue thereafter. A replication-deficient retrovirus was used to mediate pCMF1 antisense expression in cardiogenic mesoderm. These analyses determined that the presence of pCMF1 antisense sequences disrupted myosin heavy chain expression during cardiac mesoderm differentiation. pCMF1 antisense had no effect on myosin heavy chain expression in differentiated cardiac myocytes. These data suggest a potential function for pCMF1 during cardiac myogenesis.

Sign in / Sign up

Export Citation Format

Share Document