Selective Differentiation into Hematopoietic and Cardiac Cells from Pluripotent Stem Cells Based on the Expression of Cell Surface Markers

2015 ◽  
pp. 181-195 ◽  
Author(s):  
Atsumasa Okada ◽  
Katsuhisa Tashiro ◽  
Tomoko Yamaguchi ◽  
Kenji Kawabata
Keyword(s):  
Stem Cells ◽  
Cell Surface ◽  
Pluripotent Stem Cells ◽  
Cardiac Cells ◽  
Surface Markers ◽  
Cell Surface Markers ◽  
Selective Differentiation

scholarly journals Cell surface markers for the identification and study of human naive pluripotent stem cells

2018 ◽  
Vol 26 ◽  
pp. 36-43 ◽  
Author(s):  
Oliver Trusler ◽  
Ziyi Huang ◽  
Jacob Goodwin ◽  
Andrew L. Laslett
Keyword(s):  
Stem Cells ◽  
Cell Surface ◽  
Pluripotent Stem Cells ◽  
Surface Markers ◽  
Cell Surface Markers

scholarly journals p53 Is a Crucial Regulator of Hemogenic Endothelial Cell Differentiation from Human Induced Pluripotent Stem Cells

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 1085-1085
Author(s):  
Jitendra K. Kanaujiya ◽  
Elizabeth G. Lingenheld ◽  
William C. Skarnes ◽  
Hideyuki Oguro
Keyword(s):  
Stem Cells ◽  
Cell Surface ◽  
Pluripotent Stem Cells ◽  
Surface Markers ◽  
Cell Surface Markers ◽  
Hematopoietic Differentiation ◽  
Hematopoietic Stem ◽  
Scientific Advisory ◽  
Induced Pluripotent

Abstract De novo generation of hematopoietic stem cells (HSCs) from human induced pluripotent stem cells (hiPSCs) could provide a virtually unlimited supply of autologous HSCs for clinical transplantation, and offer various approaches that enable gene therapy, drug discovery, disease modeling, and in vitro modeling of human hematopoietic development. However, the derivation of long-term self-renewing HSCs from hiPSCs in culture remains elusive. The tumor suppressor protein p53 plays important roles in normal and malignant hematopoiesis, and Trp53-deficient mice exhibit increased number of HSCs. Although activation of p53 is known to promote differentiation of hPSCs and hPSCs recurrently acquire TP53 dominant negative mutations, its role in hematopoietic differentiation of hiPSCs has not been explored. To differentiate hiPSCs into hematopoietic stem and progenitor cells (HSPCs), we used embryoid body (EB) formation method to first differentiate hiPSCs into hemogenic endothelial (HE) cells that express the CD34 highCD144 +CD73 -CD184 -CD43 -CD235a - cell-surface markers. HE cells were then transferred onto a Matrigel-coated plate to undergo endothelial-to-hematopoietic transition (EHT) to generate HSPCs that express the CD34 midCD45 mid cell-surface markers. Developed HSPCs were functionally evaluated by colony forming assay. We observed that the expression of CDKN1A, a p53 target gene, was upregulated in hiPSC-derived EBs and HSPCs over the course of differentiation. To investigate the role of p53 in the generation of HSPCs from hiPSCs, we genetically deleted TP53 in hiPSCs followed by hematopoietic differentiation. While TP53 deletion increased the growth of EBs, it resulted in severe impairment of differentiation into HE cells and overall production of HSPCs that can form colonies. During HE differentiation from hiPSCs, TP53-deficient EBs showed significant reduction of endothelial-lineage gene expression, such as ETV2, CDH5, and PECAM1, as well as expression of RUNX1, a master transcription factor required for HE specification. These results indicate the indispensable role of p53 in HE differentiation from hiPSCs. We then examined the effect of p53 activation on HE differentiation from hiPSCs by pharmacological activation of p53 in hiPSC-derived cells. Transient activation of p53 by Nutlin-3, a small molecule that inhibits the p53-HDM2 interaction and protects p53 from proteasomal degradation, only during HE differentiation but not during EHT significantly promoted HSPC generation as compared to the vehicle treated control. Our findings shed light on the importance of selecting hiPSC lines that retain normal p53 activity for HE differentiation, and provide an approach to promote hematopoietic differentiation of hiPSCs by transiently activating p53 during HE differentiation. Disclosures Kanaujiya: Synthego: Other: Scientific Advisory; eGenesis: Other: Scientific Advisory.

Neonatal stem cells exhibit specific characteristics in function, proliferation, and cellular signaling that distinguish them from their adult counterparts

2008 ◽  
Vol 294 (5) ◽  
pp. R1491-R1497 ◽  
Author(s):  
Troy A. Markel ◽  
Meijing Wang ◽  
Paul R. Crisostomo ◽  
Maiuxi C. Manukyan ◽  
Jeffrey A. Poynter ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Surface ◽  
Surface Markers ◽  
Cell Surface Markers ◽  
Local Inflammatory Response ◽  
Cell Counts ◽  
Marrow Mesenchymal Stem Cells ◽  
Growth Factor Production ◽  
Erk Inhibition ◽  
Different Levels

Stem cells may be a novel treatment modality for organ ischemia, possibly through beneficial paracrine mechanisms. Stem cells from older hosts have been shown to exhibit decreased function during stress. We therefore hypothesized that 1) neonatal bone marrow mesenchymal stem cells (nBMSCs) would produce different levels of IL-6, VEGF, and IGF-1 compared with adults (aBMSCs) when stimulated with TNF or LPS; 2) differences in cytokines would be due to distinct cellular characteristics, such as proliferation or pluripotent potential; and 3) differences in cytokines would be associated with differences in p38 MAPK and ERK signaling within nBMSCs. BMSCs were isolated from adult and neonatal mice. Cells were exposed to TNF or LPS with or without p38 or ERK inhibition. Growth factors were measured via ELISA, proliferation via daily cell counts, cell surface markers via flow cytometry, and pluripotent potential via alkaline phosphatase activity. nBMSCs produced lower levels of IL-6 and VEGF, but higher levels of IGF-1 under basal conditions, as well as after stimulation with TNF, but not LPS. Neonatal and adult BMSCs had similar pluripotent potentials and cell surface markers, but nBMSCs proliferated faster. Furthermore, p38 and ERK appeared to play a more substantial role in nBMSC cytokine and growth factor production. Neonatal stem cells may aid in decreasing the local inflammatory response during ischemia, and could possibly be expanded more rapidly than adult cells prior to therapeutic use.

Cell surface markers and exogenously induced PpIX in synovial mesenchymal stem cells

2015 ◽  
Vol 87 (11) ◽  
pp. 1001-1011 ◽  
Author(s):  
Jaroslav Denkovskij ◽  
Romualdas Rudys ◽  
Eiva Bernotiene ◽  
Mindaugas Minderis ◽  
Saulius Bagdonas ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Surface ◽  
Surface Markers ◽  
Cell Surface Markers

Phenotypic analysis of cell surface markers and gene expression of human mesenchymal stem cells and chondrocytes during monolayer expansion

Biorheology ◽  
2008 ◽  
Vol 45 (3-4) ◽  
pp. 513-526 ◽  
Author(s):  
Christel Cournil-Henrionnet ◽  
Céline Huselstein ◽  
Yun Wang ◽  
Laurent Galois ◽  
Didier Mainard ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Surface ◽  
Human Mesenchymal Stem Cells ◽  
Surface Markers ◽  
Cell Surface Markers ◽  
Phenotypic Analysis ◽  
Monolayer Expansion

scholarly journals Molecular Profiling of Conjunctival Epithelial Side-Population Stem Cells: Atypical Cell Surface Markers and Sources of a Slow-Cycling Phenotype

2009 ◽  
Vol 50 (9) ◽  
pp. 4162 ◽  
Author(s):  
M. A. Murat Akinci ◽  
Helen Turner ◽  
Maria Taveras ◽  
Alex Barash ◽  
Zheng Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Surface ◽  
Side Population ◽  
Molecular Profiling ◽  
Surface Markers ◽  
Cell Surface Markers ◽  
Atypical Cell ◽  
Slow Cycling
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