scholarly journals Epigenetic mechanisms to maintain embryonic stem cell identity

2010 ◽  
Vol 32 (5) ◽  
pp. 11-13
Author(s):  
Sarah Cooper
Keyword(s):  
Stem Cell ◽  
Neurodegenerative Diseases ◽  
Embryonic Stem Cell ◽  
Tissue Regeneration ◽  
Germ Cells ◽  
Es Cells ◽  
Embryonic Stem ◽  
The Body ◽  
Epigenetic Mechanisms ◽  
External Signals

Advocates of embryonic stem (ES) cells have promised much from this technology, from reversal of neurodegenerative diseases to custom tissue regeneration. What is it, then, that makes ES cells so remarkable? Essentially, this question can be answered by two major features: an ability to self-renew and thereby divide indefinitely in culture, and pluripotency, the ability to respond to external signals and differentiate into any type of cell in the body, including germ cells.

scholarly journals Complete Meiosis from Embryonic Stem Cell-Derived Germ Cells In Vitro

2016 ◽  
Vol 18 (3) ◽  
pp. 330-340 ◽  
Author(s):  
Quan Zhou ◽  
Mei Wang ◽  
Yan Yuan ◽  
Xuepeng Wang ◽  
Rui Fu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Embryonic Stem Cell ◽  
Germ Cells ◽  
Embryonic Stem

scholarly journals SIRT1 Deficiency Compromises Mouse Embryonic Stem Cell Differentiation, and Embryonic and Adult Hematopoiesis In the Mouse.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1612-1612
Author(s):  
Xuan Ou ◽  
Hee-Don Chae ◽  
Rui-Hong Wang ◽  
William C Shelley ◽  
Scott Cooper ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Differentiation ◽  
Embryonic Stem Cell ◽  
Conflicts Of Interest ◽  
Es Cells ◽  
Embryonic Stem ◽  
Stem Cell Differentiation ◽  
Embryonic Stem Cell Differentiation ◽  
Erythroid Progenitors ◽  
Erythroid Progenitor

Abstract Abstract 1612 SIRT1 is a conserved NAD-dependent deacetylase capable of deacetylating a number of protein substrates including, but not limited to, p53 and FOXO transcription factors. SIRT1 plays an important role in a variety of biological processes including stress resistance, metabolism, differentiation and aging (Rodgers et al, Nature, 2005; 434:113). SIRT1 is expressed at high levels in mouse embryos. A role for SIRT1 in mouse (m) embryonic stem cell (ESC) maintenance and differentiation is only beginning to be elucidated (Han et al, Cell Stem Cell, 2008; 2:241, Calvanese V et al, PNAS, 2010; 10713736). Here we focus on a role for SIRT1 in differentiation of mESCs into hematopoietic progenitors (HPCs), and in embryonic and adult hematopoiesis. We hypothesized that SIRT1 is involved in hematopoietic commitment within the mouse. We initially assessed the ability of WT and SIRT1-/- mESC to give rise to blast colony forming cells (BL-CFC), a transient population that is present in EBs between day 2.5 and day 3.5 of differentiation and represents the in vitro equivalent of the hemangioblast and as such, the earliest commitment step in the differentiation of mesoderm to the hematopoietic and endothelial lineages. SIRT1-/- ESCs exhibited markedly delayed formation of BL-CFC. The emergence of the Flk-1+/c-Kit- cell population pattern was also delayed, consistent with the delayed pattern of BL-CFC development in SIRT1-/- EBs. This observed delay appears to result from a slower differentiation of the SIRT1-/- ESCs as the kinetics of decline in secondary EB potential, an indication of undifferentiated ES cells, is delayed compared to that of SIRT1+/+ ES cells. When analyzed for hematopoietic and endothelial potential of individual blast colony, replated SIRT1-/- BL-CFC presented limited hematopoietic potential, whereas endothelial potential was essentially unaltered. Next, the ability of SIRT1-/- ESCs to form primitive and definitive hematopoietic cells was evaluated and we found that primitive erythroid progenitors formed from SIRT1-/- R1 cells were not only delayed but greatly decreased. Moreover, after differentiation of SIRT1 -/- mESC there were also significant decreases in granulocyte-macrophage (CFU-GM), and multipotential (CFU-GEMM) progenitors. Differences in primitive and definitive erythroid progenitors were confirmed by gene analysis of βH1 globin (embryonic hemoglobin), a marker for primitive erythroid cells, and βmajor globin (adult hemoglobin). The above delay defects were associated with delayed ability to switch off Oct4, Nanog and Fgf5, decreased β-H1 Globin, β-major globin, Scl gene expression and reduced activation of the Erk1/2 pathway upon SIRT1-/- ESC commitment. Reintroduction of WT SIRT1 into SIRT1-/- cells partially rescued the primitive erythroid progenitor formation of SIRT1-/- cells and the expression of hemoglobin genes, Hbb-bh1 and Hbb-b1, suggesting that the defect of hematopoietic commitment is due to deletion of SIRT1, and not to genetic drifting of SIRT1-/- cells. To confirm SIRT1 effects, we assessed embryonic and adult hematopoiesis in SIRT1+/+, +/− and -/- mice. Yolk sacs from SIRT1 mutant embryos generated fewer primitive erythorid precursors compared to wild-type and heterozygous mice. Moreover, knockout of SIRT1 decreased primary bone marrow HPCs in 5 week and 12 month old mice, effects especially notable at lower (5%) O2 tension. Taken together, these results demonstrate that SIRT1 plays a role in mouse embryonic and adult stem cell differentiation. Disclosures: No relevant conflicts of interest to declare.

Cloning Animals, Cells, and Genes

2017 ◽  
pp. 129-150
Author(s):  
Scott Gilbert
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Embryonic Stem Cells ◽  
Embryonic Stem Cell ◽  
New Technology ◽  
Embryonic Stem ◽  
The Body ◽  
Animal Cloning ◽  
Medical Task

Every technology has its history, and this chapter looks at the technologies of animal cloning and how they changed when it became apparent that one could perform some of the medical task of cloning with embryonic stem cells. These stem cells were difficult to obtain (and morally worrisome to many) and a new technology, induced pluripotential stem cells, enabled researchers to transform nearly any cell of the body into an embryonic stem cell. This has brought new worries concerning the ability to manipulate these cells to enhance a person’s capabilities.

Role of TPO in the Differentiation of Embryonic Stem Cells into Hematopoetic Cells.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4202-4202
Author(s):  
Zheng Wang ◽  
Pramono Andri ◽  
Skokowa Julia ◽  
Welte Karl
Keyword(s):  
Stem Cell ◽  
Cell Differentiation ◽  
Rhesus Monkey ◽  
Embryonic Stem Cell ◽  
Mrna Expression ◽  
Es Cells ◽  
Embryonic Stem ◽  
Stem Cell Differentiation ◽  
Embryonic Stem Cell Differentiation

Abstract Thrombopoetin (TPO) is a primary regulator of megakaryocyte and platelet production. However, studies in c-mpl-deficient mice and in congenital amegakaryocytic thrombocytopenia-patients with non-sense c-mpl mutation who develop pancytopenia during the first years of life suggest that TPO also play an important role on early hematopoesis. We demonstrated that TPO enhances FLK-1 (VEGF-receptor) expression on hemangioblasts during murine embryonic stem cell differentiation in embryoid body-liquid cultures (up to 73%). To extend our studies, we investigated the TPO signaling in FLK-1 positive cells. ES cells at different time point of differentiation showed that TPO enhances c-mpl-, BMP4-, Notch-, HOXB4-, HOXB9-, HOXA10-, Runx1-and CD133- mRNA expression. To investigate mesoderm formation, we also analyzed GATA-4 and T-brachyury mRNA level expression. Interestingly, we found that TPO alone did not increase GATA-4- and T-brachyury- mRNA expression, suggesting that TPO requires other cytokines to form the mesoderm. We also found that TPO could maintain VEGF-A mRNA expression level during differentiation of ES-cells. We hypothesize that VEGF expression together with c-mpl expression is required in hematopoetic differentiation of ES cell. This activity of Tpo was also observed during Rhesus monkey embryonic stem cell differentiation into hematopoetic cell. Only combinations of TPO and VEGF were capable of increasing CD34 positive hematopoietic progenitor cells (up to 8%), but TPO alone failed to induce high levels of CD34+ cell. In addition, analysis of gene expression during hemangioblast development demonstrated that TPO was capable of increasing the expression of VEGF receptors (FLK-1) and TPO receptors (c-mpl) in mice and primates. The in-vitro differentiation of mouse and rhesus monkey ES cells provides an opportunity to better understand the role of TPO in the early stage of hematopoietic development from ES cells to mature hematopoietic cells.

scholarly journals Embryonic stem cell-derived extracellular vesicles promote the recovery of kidney injury

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lu Yu ◽  
Siying Liu ◽  
Chen Wang ◽  
Chuanyu Zhang ◽  
Yajie Wen ◽  
...  
Keyword(s):  
Stem Cell ◽  
Embryonic Stem Cell ◽  
Extracellular Vesicles ◽  
Therapeutic Potential ◽  
Es Cells ◽  
Ischemia Reperfusion ◽  
Embryonic Stem ◽  
Kidney Injury ◽  
Structure And Function ◽  
And Function

Abstract Background Embryonic stem cell-derived extracellular vesicles (ESC-EVs) possess therapeutic potential for a variety of diseases and are considered as an alternative of ES cells. Acute kidney injury (AKI) is a common acute and severe disease in clinical practice, which seriously threatens human life and health. However, the roles and mechanisms of ESC-EVs on AKI remain unclear. Methods In this study, we evaluated the effects of ESC-EVs on physiological repair and pathological repair using murine ischemia-reperfusion injury-induced AKI model, the potential mechanisms of which were next investigated. EVs were isolated from ESCs and EVs derived from mouse fibroblasts as therapeutic controls. We then investigated whether ESC-EVs can restore the structure and function of the damaged kidney by promoting physiological repair and inhibiting the pathological repair process after AKI in vivo and in vitro. Results We found that ESC-EVs significantly promoted the recovery of the structure and function of the damaged kidney. ESC-EVs increased the proliferation of renal tubular epithelial cells, facilitated renal angiogenesis, inhibited the progression of renal fibrosis, and rescued DNA damage caused by ischemia and reperfusion after AKI. Finally, we found that ESC-EVs play a therapeutic effect by activating Sox9+ cells. Conclusions ESC-EVs significantly promote the physiological repair and inhibit the pathological repair after AKI, enabling restoration of the structure and function of the damaged kidney. This strategy might emerge as a novel therapeutic strategy for ESC clinical application.

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