Isolation of mutants showing temperature-sensitive cell growth from embryonal carcinoma cells: Control of stem cell differentiation by incubation temperatures

1989 ◽  
Vol 165 (1) ◽  
pp. 65-72 ◽  
Author(s):  
Yoshitake Nishimune ◽  
Yukio Nishina ◽  
Tetsuro Sumi ◽  
Mitsuko Kosaka ◽  
Masashi Takeda ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Differentiation ◽  
Cell Growth ◽  
Embryonal Carcinoma ◽  
Stem Cell Differentiation ◽  
Carcinoma Cells ◽  
Temperature Sensitive ◽  
Embryonal Carcinoma Cells ◽  
Sensitive Cell ◽  
Incubation Temperatures

Analysis of cell-differentiation lineage in human teratomas using new monoclonal antibodies to cytostructural antigens of embryonal carcinoma cells

1988 ◽  
Vol 39 (2) ◽  
pp. 139-149 ◽  
Author(s):  
Martin F. Pera ◽  
Maria Jose Blasco-Lafita ◽  
Susan Cooper ◽  
Malcolm Mason ◽  
Judith Mills ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Cell Differentiation ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells

scholarly journals Maintenance of active chromatin states by HMGN2 is required for stem cell identity in a pluripotent stem cell model

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Sylvia Garza-Manero ◽  
Abdulmajeed Abdulghani A. Sindi ◽  
Gokula Mohan ◽  
Ohoud Rehbini ◽  
Valentine H. M. Jeantet ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Neuronal Differentiation ◽  
Embryonal Carcinoma ◽  
Cell Model ◽  
Carcinoma Cells ◽  
Adult Brain ◽  
Embryonal Carcinoma Cells ◽  
Stem Cell Model ◽  
Neural Stem Progenitor Cells

Abstract Background Members of the HMGN protein family modulate chromatin structure and influence epigenetic modifications. HMGN1 and HMGN2 are highly expressed during early development and in the neural stem/progenitor cells of the developing and adult brain. Here, we investigate whether HMGN proteins contribute to the chromatin plasticity and epigenetic regulation that is essential for maintaining pluripotency in stem cells. Results We show that loss of Hmgn1 or Hmgn2 in pluripotent embryonal carcinoma cells leads to increased levels of spontaneous neuronal differentiation. This is accompanied by the loss of pluripotency markers Nanog and Ssea1, and increased expression of the pro-neural transcription factors Neurog1 and Ascl1. Neural stem cells derived from these Hmgn-knockout lines also show increased spontaneous neuronal differentiation and Neurog1 expression. The loss of HMGN2 leads to a global reduction in H3K9 acetylation, and disrupts the profile of H3K4me3, H3K9ac, H3K27ac and H3K122ac at the Nanog and Oct4 loci. At endodermal/mesodermal genes, Hmgn2-knockout cells show a switch from a bivalent to a repressive chromatin configuration. However, at neuronal lineage genes whose expression is increased, no epigenetic changes are observed and their bivalent states are retained following the loss of HMGN2. Conclusions We conclude that HMGN1 and HMGN2 maintain the identity of pluripotent embryonal carcinoma cells by optimising the pluripotency transcription factor network and protecting the cells from precocious differentiation. Our evidence suggests that HMGN2 regulates active and bivalent genes by promoting an epigenetic landscape of active histone modifications at promoters and enhancers.

Abstract 386: Sonic Hedgehog Promotes Stem Cell Differentiation to Vascular Smooth Muscle in vitro

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Maryam Alshamrani ◽  
Emma Fitzpatrick ◽  
Eileen M Redmond ◽  
Paul A Cahill
Keyword(s):  
Bone Marrow ◽  
Smooth Muscle ◽  
Stem Cell ◽  
Cell Differentiation ◽  
Cell Growth ◽  
Vascular Smooth Muscle ◽  
Sonic Hedgehog ◽  
Stem Cell Differentiation ◽  
Differentiation Marker

Background: The morphogen Sonic Hedgehog (SHh) and its signaling pathway components are significantly up-regulated within adventitial and medial segments from arteriosclerotic vessels in mice concomitant with enhanced accumulation of SMCs. This vessel remodelling is attenuated in vivo following Hh receptor, Patched 1, depletion. There is evidence supporting a role for stem cell-derived vascular smooth muscle (vSMCs) in contributing to arteriosclerotic vascular disease. In this context, SHh signaling may be an important regulator of stem cell self-renewal and differentiation to SMC in vitro. Aim: Determine the effects of SHh on bone-marrow derived mesenchymal stem cell (MSC) differentiation to SMC in vitro. Methods: Murine CD44+ bone-marrow derived MSCs and Sca1+ rat adventitial progenitor stem cells (APCs) were examined for SHh components and their capacity to differentiate to SMCs before and after treatment with sonic hedgehog (rSHh, 0.5 μg/ml) for 7 d, in the absence or presence of Hh inhibitors cyclopamine (10μM) or HPI-4 (50μM). The transition to SMC was determined be examining intermediate (calponin1, CNN1) and late (myosin heavy chain, Myh11) SMC differentiation marker expression by western blot analysis and immunocytochemistry, respectively. Results: Hh signaling components were present on MSCs and APCs. Stem cell growth was unaffected by treatment with Hh inhibitors cyclopamine or HPI-4 at concentrations that inhibited Gli signalling in vitro. Recombinant SHh increased SMC differentiation marker protein protein expression after 7 days, an effect that was inhibited following SHh inhibition with smoothened inhibitors cyclopamine and HPI-4. Conclusion: in the absence of any effect on cell growth, Sonic Hedgehog controls mesenchymal stem-like cell differentiation to SMC.

scholarly journals Switched alternative splicing of oncogene CoAA during embryonal carcinoma stem cell differentiation

2007 ◽  
Vol 35 (6) ◽  
pp. 1919-1932 ◽  
Author(s):  
Zheqiong Yang ◽  
Yang Sui ◽  
Shiqin Xiong ◽  
Sean S. Liour ◽  
Andrew C. Phillips ◽  
...  
Keyword(s):  
Stem Cell ◽  
Alternative Splicing ◽  
Cell Differentiation ◽  
Embryonal Carcinoma ◽  
Stem Cell Differentiation
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