Pluripotency maintenance mechanism of embryonic stem cells and reprogramming
Division of Molecular Biology and Cell Engineering, Department of Regenerative Medicine, Research Institute, International Medical Center of Japan, 1-21-1 Toyama, Shinjuku-ku, Tokyo 162-8655, Japan. International journal of hematology
(Impact Factor: 1.92).
02/2010; 91(3):360-72. DOI: 10.1007/s12185-010-0517-9
Embryonic stem (ES) cells are derived from blastocysts and are pluripotent. This pluripotency has attracted the interest of numerous researchers, both to expand our fundamental understanding of developmental biology and also because of potential applications in regenerative medicine. Systems biological studies have demonstrated that the pivotal transcription factors form a network. There they activate pluripotency-associated genes, including themselves, while repressing the developmentally regulated genes through co-occupation with various protein complexes. The chromatin structure characteristic of ES cells also contributes to the maintenance of the network. In this review, I focus on recent advances in our understanding of the transcriptional network that maintains pluripotency in mouse ES cells.
Available from: Pablo F Argibay
- "Some experiments have shown that loss of Erk2 suppresses differentiation in embryonic stem cells. Erk inhibition was reported to allow the derivation of mESCs even from nonpermissive mouse strains, and one possibility is that KoSR maintains the activity of this enzyme at low levels, facilitating mES cells isolation (Bryja et al., 2006; Buehr and Smith, 2003; Masui, 2010). Some authors have attempted supplementation of ES medium with a FBS-KoSR mixture in different ratios to improve the isolation and the subsequent establishment of ESCs (Lee et al., 2006; Tanimoto et al., 2008). "
Available from: Annalisa Fico
- "This enables catenin beta 1 (Ctnnb1) to traslocate into the nucleus to form the Ctnnb1/Tcf complex, which in turn activates the downstream genes (Willert and Jones, 2006). In the presence of Wnt signalling, transcription factor (Tcf3) activates the downstream genes that promote pluripotency maintenance by collaborating with the pivotal transcription factors Otc3/4 (Fig. 2), Sox2 and Nanog (Masui, 2010). "
Available from: Hee-Don Chae
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ABSTRACT: SIRT1 is a founding member of a sirtuin family of 7 proteins and histone deacetylases. It is involved in cellular resistance to stress, metabolism, differentiation, aging, and tumor suppression. SIRT1(-/-) mice demonstrate embryonic and postnatal development defects. We examined hematopoietic and endothelial cell differentiation of SIRT1(-/-) mouse embryonic stem cells (ESCs) in vitro, and hematopoietic progenitors in SIRT1(+/+)(+/-), and (-/-) mice. SIRT1(-/-) ESCs formed fewer mature blast cell colonies. Replated SIRT1(-/-) blast colony-forming cells demonstrated defective hematopoietic potential. Endothelial cell production was unaltered, but there were defects in formation of a primitive vascular network from SIRT1(-/-)-derived embryoid bodies. Development of primitive and definitive progenitors derived from SIRT1(-/-) ESCs were also delayed and/or defective. Differentiation delay/defects were associated with delayed capacity to switch off Oct4, Nanog and Fgf5 expression, decreased β-H1 globin, β-major globin, and Scl gene expression, and reduced activation of Erk1/2. Ectopic expression of SIRT1 rescued SIRT1(-/-) ESC differentiation deficiencies. SIRT1(-/-) yolk sacs manifested fewer primitive erythroid precursors. SIRT1(-/-) and SIRT1(+/-) adult marrow had decreased numbers and cycling of hematopoietic progenitors, effects more apparent at 5%, than at 20%, oxygen tension, and these progenitors survived less well in vitro under conditions of delayed growth factor addition. This suggests a role for SIRT1 in ESC differentiation and mouse hematopoiesis.
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