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Hemangioblast skewing from embryonic stem(ES) cells by defined factors

ABSTRACT: Successful derivation of a specific cell lineage from pluripotent stem cells will tremendously facilitate the clinical usage of pluripotent stem derived somatic cells. Herein, we demonstrate that ER71/Etv2, GATA2 and Scl form a core network in hemangioblast development and that transient co-expression of these three factors robustly induced hemangioblasts from ES cells. Such induced hemangioblasts potently generated hematopoietic and endothelial cells in culture as well as in vivo, warranting the evaluation of these cells in the future for repairing and/or regenerating hematopoietic and/or angiogenic defects. We have established a doxycycline inducible ES cell, iEGS, in which ER71/Etv2, GATA2 three transcription factors can be transiently co-expressed by doxycycline induction. We further analyzed the downstream target genes and signaling pathways at 6, 12 and 24hrs after ER71/Etv2, GATA2 induction. These data were obtained from three independent experiments.

ORGANISM(S): Mus musculus

SUBMITTER: Fang Liu 

PROVIDER: E-GEOD-45147 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Enhanced hemangioblast generation and improved vascular repair and regeneration from embryonic stem cells by defined transcription factors.

Liu Fang F   Bhang Suk Ho SH   Arentson Elizabeth E   Sawada Atsushi A   Kim Chan Kyu CK   Kang Inyoung I   Yu Jinsheng J   Sakurai Nagisa N   Kim Suk Hyung SH   Yoo Judy Ji Woon JJ   Kim Paul P   Pahng Seong Ho SH   Xia Younan Y   Solnica-Krezel Lilianna L   Choi Kyunghee K  

Stem cell reports 20130725 2

The fetal liver kinase 1 (FLK-1)(+) hemangioblast can generate hematopoietic, endothelial, and smooth muscle cells (SMCs). ER71/ETV2, GATA2, and SCL form a core transcriptional network in hemangioblast development. Transient coexpression of these three factors during mesoderm formation stage in mouse embryonic stem cells (ESCs) robustly enhanced hemangioblast generation by activating bone morphogenetic protein (BMP) and FLK-1 signaling while inhibiting phosphatidylinositol 3-kinase, WNT signalin  ...[more]

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