scholarly journals High density cultures of embryoid bodies enhanced cardiac differentiation of murine embryonic stem cells

2011 ◽  
Vol 416 (1-2) ◽  
pp. 51-57 ◽  
Author(s):  
Min Young Lee ◽  
Esra Cagavi Bozkulak ◽  
Simon Schliffke ◽  
Peter J. Amos ◽  
Yongming Ren ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Embryoid Bodies ◽  
High Density ◽  
Cardiac Differentiation ◽  
Murine Embryonic Stem Cells

scholarly journals Delayed Mesoderm and Erythroid Differentiation of Murine Embryonic Stem Cells in the Absence of the Transcriptional Regulator FUBP1

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Josephine Wesely ◽  
Marlene Steiner ◽  
Frank Schnütgen ◽  
Manuel Kaulich ◽  
Michael A. Rieger ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Early Time ◽  
Transcriptional Regulator ◽  
Erythroid Differentiation ◽  
Embryoid Bodies ◽  
Hematopoietic Stem ◽  
Murine Embryonic Stem Cells ◽  
Delayed Differentiation

The transcriptional regulator far upstream binding protein 1 (FUBP1) is essential for fetal and adult hematopoietic stem cell (HSC) self-renewal, and the constitutive absence of FUBP1 activity during early development leads to embryonic lethality in homozygous mutant mice. To investigate the role of FUBP1 in murine embryonic stem cells (ESCs) and in particular during differentiation into hematopoietic lineages, we generated Fubp1 knockout (KO) ESC clones using CRISPR/Cas9 technology. Although FUBP1 is expressed in undifferentiated ESCs and during spontaneous differentiation following aggregation into embryoid bodies (EBs), absence of FUBP1 did not affect ESC maintenance. Interestingly, we observed a delayed differentiation of FUBP1-deficient ESCs into the mesoderm germ layer, as indicated by impaired expression of several mesoderm markers including Brachyury at an early time point of ESC differentiation upon aggregation to EBs. Coculture experiments with OP9 cells in the presence of erythropoietin revealed a diminished differentiation capacity of Fubp1 KO ESCs into the erythroid lineage. Our data showed that FUBP1 is important for the onset of mesoderm differentiation and maturation of hematopoietic progenitor cells into the erythroid lineage, a finding that is supported by the phenotype of FUBP1-deficient mice.

scholarly journals Effects of Puerarin on Cardiac Differentiation and Ventricular Specialization of Murine Embryonic Stem Cells

2013 ◽  
Vol 32 (4) ◽  
pp. 789-800 ◽  
Author(s):  
Ying Cheng ◽  
Lu Wang ◽  
Ming Tang ◽  
Mengmeng Yin ◽  
Yurong Cui ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Cardiac Differentiation ◽  
Murine Embryonic Stem Cells

scholarly journals Nitro-Oleic Acid Inhibits Stemness Maintenance and Enhances Neural Differentiation of Mouse Embryonic Stem Cells via STAT3 Signaling

2021 ◽  
Vol 22 (18) ◽  
pp. 9981
Author(s):  
Jana Pereckova ◽  
Michaela Pekarova ◽  
Nikoletta Szamecova ◽  
Zuzana Hoferova ◽  
Kristyna Kamarytova ◽  
...  
Keyword(s):  
Stem Cells ◽  
Transcription Factor ◽  
Oleic Acid ◽  
Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Embryoid Bodies ◽  
Cardiac Differentiation ◽  
Class Iii ◽  
Stat3 Phosphorylation ◽  
Stem Cell Pluripotency

Nitro-oleic acid (NO2-OA), pluripotent cell-signaling mediator, was recently described as a modulator of the signal transducer and activator of transcription 3 (STAT3) activity. In our study, we discovered new aspects of NO2-OA involvement in the regulation of stem cell pluripotency and differentiation. Murine embryonic stem cells (mESC) or mESC-derived embryoid bodies (EBs) were exposed to NO2-OA or oleic acid (OA) for selected time periods. Our results showed that NO2-OA but not OA caused the loss of pluripotency of mESC cultivated in leukemia inhibitory factor (LIF) rich medium via the decrease of pluripotency markers (NANOG, sex-determining region Y-box 1 transcription factor (SOX2), and octamer-binding transcription factor 4 (OCT4)). The effects of NO2-OA on mESC correlated with reduced phosphorylation of STAT3. Subsequent differentiation led to an increase of the ectodermal marker orthodenticle homolog 2 (Otx2). Similarly, treatment of mESC-derived EBs by NO2-OA resulted in the up-regulation of both neural markers Nestin and β-Tubulin class III (Tubb3). Interestingly, the expression of cardiac-specific genes and beating of EBs were significantly decreased. In conclusion, NO2-OA is able to modulate pluripotency of mESC via the regulation of STAT3 phosphorylation. Further, it attenuates cardiac differentiation on the one hand, and on the other hand, it directs mESC into neural fate.

BMP4 Favors Hematopoietic Differentiation from Murine Embryonic Stem Cells and Acts by Activation of the cdx-hox Pathway.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3613-3613
Author(s):  
Claudia Lengerke ◽  
Yuan Wang ◽  
Frank Yates ◽  
Leila Maouche-Chretien ◽  
George Q. Daley
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Hox Genes ◽  
Embryonic Stem ◽  
Embryoid Bodies ◽  
Hematopoietic Stem ◽  
Hox Gene ◽  
Murine Embryonic Stem Cells

Abstract Cdx4 and cdx1, members of the caudal family of homeodomain-containing transcriptional regulators, are important for specifying the hematopoietic fate of mesoderm in the zebrafish. We have shown that the cdx4 gene plays a role in enhancing hematopoietic fate during in vitro differentiation of murine ESCs (Davidson et al., Nature 2003). Cdx4 induces hox genes, and genetic modification of mESCs with a combination of cdx4 and hoxb4 promotes long-term engraftment of ESC-derived HSCs in lethally irradiated primary and secondary mice (Wang et al, submitted). While cdx1 is known to be a direct target of signaling by the embryonic morphogens fgf, wnt3a, and retinoids, morphogens acting upstream of cdx4 have not yet been defined. Our goal is to determine optimal morphogen conditions for hematopoietic commitment from murine embryonic stem cells by evaluating activation of the cdx-hox pathway. We have developed quantitative RT-PCR assays for the cdx genes (cdx4, cdx1 and cdx2) and multiple hox genes as well as markers specific to hematopoietic stem cells and lineages. We have used these assays, together with a reporter line engineered to express GFP from the brachury locus (Fehling et al., Development 2003), to characterize the conditions for mesodermal induction and hematopoietic fate specification following addition of morphogens to differentiating cultures of ES cells under serum-free conditions. Among all morphogens tested (BMP4, activin, nodal, wnt3a, wnt5a, sonic hedgehog, indian hedgehog, retinoic acid), only BMP4 has been found to strongly induce CDX4 gene expression within the developing embryoid bodies, while addition of the BMP4 inhibitor noggin to serum suppressed CDX4 expression. Addition of BMP4 significantly increases the number of emerging CD41+ and CD45+ cells, the precursors of definitive hematopoietic stem cells. We are currently analyzing the functional changes following BMP4 exposure, and correlating hematopoietic maturation with changes in the Hox gene expression pattern. Analysis of the cdx-hox gene pathway provides a means of otpimizing induction of hematopoietic fate by application of embryonic morphogens.

scholarly journals Cardiopoietic programming of embryonic stem cells for tumor-free heart repair

2007 ◽  
Vol 204 (2) ◽  
pp. 405-420 ◽  
Author(s):  
Atta Behfar ◽  
Carmen Perez-Terzic ◽  
Randolph S. Faustino ◽  
D. Kent Arrell ◽  
Denice M. Hodgson ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Embryonic Stem Cells ◽  
Nuclear Translocation ◽  
Embryonic Stem ◽  
Embryoid Bodies ◽  
Cardiac Differentiation ◽  
Cardiac Progenitors ◽  
Tnf Α

Embryonic stem cells have the distinct potential for tissue regeneration, including cardiac repair. Their propensity for multilineage differentiation carries, however, the liability of neoplastic growth, impeding therapeutic application. Here, the tumorigenic threat associated with embryonic stem cell transplantation was suppressed by cardiac-restricted transgenic expression of the reprogramming cytokine TNF-α, enhancing the cardiogenic competence of recipient heart. The in vivo aptitude of TNF-α to promote cardiac differentiation was recapitulated in embryoid bodies in vitro. The procardiogenic action required an intact endoderm and was mediated by secreted cardio-inductive signals. Resolved TNF-α–induced endoderm-derived factors, combined in a cocktail, secured guided differentiation of embryonic stem cells in monolayers produce cardiac progenitors termed cardiopoietic cells. Characterized by a down-regulation of oncogenic markers, up-regulation, and nuclear translocation of cardiac transcription factors, this predetermined population yielded functional cardiomyocyte progeny. Recruited cardiopoietic cells delivered in infarcted hearts generated cardiomyocytes that proliferated into scar tissue, integrating with host myocardium for tumor-free repair. Thus, cardiopoietic programming establishes a strategy to hone stem cell pluripotency, offering a tumor-resistant approach for regeneration.

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