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10.1002/stem.1521 http://scihub22266oqcxt.onion/10.1002/stem.1521 C4886558!4886558 !23963623     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23963623 &cmd=llinks): Failed to open stream: HTTP request failed! 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Akt suppression of TGF? signaling contributes to the maintenance of vascular identity in embryonic stem cell-derived endothelial cells |pdf=|usr=}}{{23963623 }} gab.com Text Akt suppression of TGF signaling contributes to the maintenance of vascular identity in embryonic stem cell-derived endothelial cells JO: Stem Cells http://www.kidney.de/pget.php?&tw=1&pmid=23963623 #FOAvip The ability to generate and maintain stable in vitro cultures of mouse endothelial cells (ECs) has great potential for genetic dissection of the numerous pathologies involving vascular dysfunction as well as therapeutic applications. However, previous efforts at achieving sustained cultures of primary stable murine vascular cells have fallen short, and the cellular requirements for EC maintenance in vitro remain undefined. In this study, we have generated vascular ECs from mouse embryonic stem (ES) cells and show that active Akt is essential to their survival and propagation as homogeneous monolayers in vitro. These cells harbor the phenotypical, biochemical, and functional characteristics of ECs and expand throughout long-term cultures, while maintaining their angiogenic capacity. Moreover, Akt-transduced embryonic ECs form functional perfused vessels in vivo that anastomose with host blood vessels. We provide evidence for a novel function of Akt in stabilizing EC identity, whereby the activated form of the protein protects mouse ES cell-derived ECs from TGF?-mediated transdifferentiation by downregulating SMAD3. These findings identify a role for Akt in regulating the developmental potential of ES cell-derived ECs and demonstrate that active Akt maintains endothelial identity in embryonic ECs by interfering with active TGF?-mediated processes that would ordinarily usher these cells to alternate fates. Twit Text FOAVip Akt suppression of TGF signaling contributes to the maintenance of vascular identity in embryonic stem cell-derived endothelial cells ????Stem Cells http://www.kidney.de/pget.php?&tw=1&pmid=23963623 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23963623 #FOAvip English Wikipedia <ref>{{Cite pmid|23963623 }}</ref> Akt suppression of TGF? signaling contributes to the maintenance of vascular identity in embryonic stem cell-derived endothelial cells #MMPMID23963623 Israely E ; Ginsberg M ; Nolan D ; Ding BS ; James D ; Elemento O ; Rafii S ; Rabbany SY Stem Cells 2014[Jan]; 32 (1 ): 177-90 PMID23963623 show ga The ability to generate and maintain stable in vitro cultures of mouse endothelial cells (ECs) has great potential for genetic dissection of the numerous pathologies involving vascular dysfunction as well as therapeutic applications. However, previous efforts at achieving sustained cultures of primary stable murine vascular cells have fallen short, and the cellular requirements for EC maintenance in vitro remain undefined. In this study, we have generated vascular ECs from mouse embryonic stem (ES) cells and show that active Akt is essential to their survival and propagation as homogeneous monolayers in vitro. These cells harbor the phenotypical, biochemical, and functional characteristics of ECs and expand throughout long-term cultures, while maintaining their angiogenic capacity. Moreover, Akt-transduced embryonic ECs form functional perfused vessels in vivo that anastomose with host blood vessels. We provide evidence for a novel function of Akt in stabilizing EC identity, whereby the activated form of the protein protects mouse ES cell-derived ECs from TGF?-mediated transdifferentiation by downregulating SMAD3. These findings identify a role for Akt in regulating the developmental potential of ES cell-derived ECs and demonstrate that active Akt maintains endothelial identity in embryonic ECs by interfering with active TGF?-mediated processes that would ordinarily usher these cells to alternate fates. |Animals [MESH] |Cell Differentiation/physiology [MESH] |Cells, Cultured [MESH] |Embryonic Stem Cells/cytology/*metabolism [MESH] |Endothelial Cells/cytology/*metabolism [MESH] |Mice [MESH] |Proto-Oncogene Proteins c-akt/*metabolism [MESH] |Signal Transduction [MESH]Akt suppression of TGF? signaling contributes to the maintenance of va(epmc).pdf DeepDyve Pubget Overpricing