<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Yung, Sun</style></author><author><style face="normal" font="default" size="100%">Ledran, Maria</style></author><author><style face="normal" font="default" size="100%">Moreno-Gimeno, Inmaculada</style></author><author><style face="normal" font="default" size="100%">Conesa, Ana</style></author><author><style face="normal" font="default" size="100%">Montaner, David</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Dimmick, Ian</style></author><author><style face="normal" font="default" size="100%">Slater, Nicholas J</style></author><author><style face="normal" font="default" size="100%">Marenah, Lamin</style></author><author><style face="normal" font="default" size="100%">Real, Pedro J</style></author><author><style face="normal" font="default" size="100%">Paraskevopoulou, Iliana</style></author><author><style face="normal" font="default" size="100%">Bisbal, Viviana</style></author><author><style face="normal" font="default" size="100%">Burks, Deborah</style></author><author><style face="normal" font="default" size="100%">Santibanez-Koref, Mauro</style></author><author><style face="normal" font="default" size="100%">Moreno, Ruben</style></author><author><style face="normal" font="default" size="100%">Mountford, Joanne</style></author><author><style face="normal" font="default" size="100%">Menendez, Pablo</style></author><author><style face="normal" font="default" size="100%">Armstrong, Lyle</style></author><author><style face="normal" font="default" size="100%">Lako, Majlinda</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Large-scale transcriptional profiling and functional assays reveal important roles for Rho-GTPase signalling and SCL during haematopoietic differentiation of human embryonic stem cells.</style></title><secondary-title><style face="normal" font="default" size="100%">Hum Mol Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Hum Mol Genet</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Acute Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Anemia, Hemolytic</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Basic Helix-Loop-Helix Transcription Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Differentiation</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Lineage</style></keyword><keyword><style  face="normal" font="default" size="100%">Cluster Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryonic Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Erythroid Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Flow Cytometry</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Hematopoietic Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Myeloid Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Paracrine Communication</style></keyword><keyword><style  face="normal" font="default" size="100%">Proto-Oncogene Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Reverse Transcriptase Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">rho GTP-Binding Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Stem Cell Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">T-Cell Acute Lymphocytic Leukemia Protein 1</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcriptome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Dec 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">20</style></volume><pages><style face="normal" font="default" size="100%">4932-46</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Understanding the transcriptional cues that direct differentiation of human embryonic stem cells (hESCs) and human-induced pluripotent stem cells to defined and functional cell types is essential for future clinical applications. In this study, we have compared transcriptional profiles of haematopoietic progenitors derived from hESCs at various developmental stages of a feeder- and serum-free differentiation method and show that the largest transcriptional changes occur during the first 4 days of differentiation. Data mining on the basis of molecular function revealed Rho-GTPase signalling as a key regulator of differentiation. Inhibition of this pathway resulted in a significant reduction in the numbers of emerging haematopoietic progenitors throughout the differentiation window, thereby uncovering a previously unappreciated role for Rho-GTPase signalling during human haematopoietic development. Our analysis indicated that SCL was the 11th most upregulated transcript during the first 4 days of the hESC differentiation process. Overexpression of SCL in hESCs promoted differentiation to meso-endodermal lineages, the emergence of haematopoietic and erythro-megakaryocytic progenitors and accelerated erythroid differentiation. Importantly, intrasplenic transplantation of SCL-overexpressing hESC-derived haematopoietic cells enhanced recovery from induced acute anaemia without significant cell engraftment, suggesting a paracrine-mediated effect.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">24</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/21937587?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Prado-Lopez, Sonia</style></author><author><style face="normal" font="default" size="100%">Conesa, Ana</style></author><author><style face="normal" font="default" size="100%">Armiñán, Ana</style></author><author><style face="normal" font="default" size="100%">Martínez-Losa, Magdalena</style></author><author><style face="normal" font="default" size="100%">Escobedo-Lucea, Carmen</style></author><author><style face="normal" font="default" size="100%">Gandia, Carolina</style></author><author><style face="normal" font="default" size="100%">Tarazona, Sonia</style></author><author><style face="normal" font="default" size="100%">Melguizo, Dario</style></author><author><style face="normal" font="default" size="100%">Blesa, David</style></author><author><style face="normal" font="default" size="100%">Montaner, David</style></author><author><style face="normal" font="default" size="100%">Sanz-González, Silvia</style></author><author><style face="normal" font="default" size="100%">Sepúlveda, Pilar</style></author><author><style face="normal" font="default" size="100%">Götz, Stefan</style></author><author><style face="normal" font="default" size="100%">O'Connor, José Enrique</style></author><author><style face="normal" font="default" size="100%">Moreno, Ruben</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Burks, Deborah J</style></author><author><style face="normal" font="default" size="100%">Stojkovic, Miodrag</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Hypoxia promotes efficient differentiation of human embryonic stem cells to functional endothelium.</style></title><secondary-title><style face="normal" font="default" size="100%">Stem Cells</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Stem Cells</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Angiopoietin-1</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">biomarkers</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Culture Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Differentiation</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Hypoxia</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">Cells, Cultured</style></keyword><keyword><style  face="normal" font="default" size="100%">Down-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryonic Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Endothelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Myocardial Infarction</style></keyword><keyword><style  face="normal" font="default" size="100%">Neovascularization, Physiologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxygen</style></keyword><keyword><style  face="normal" font="default" size="100%">Pluripotent Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Nude</style></keyword><keyword><style  face="normal" font="default" size="100%">Vascular Endothelial Growth Factor A</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Mar 31</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">28</style></volume><pages><style face="normal" font="default" size="100%">407-18</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Early development of mammalian embryos occurs in an environment of relative hypoxia. Nevertheless, human embryonic stem cells (hESC), which are derived from the inner cell mass of blastocyst, are routinely cultured under the same atmospheric conditions (21% O(2)) as somatic cells. We hypothesized that O(2) levels modulate gene expression and differentiation potential of hESC, and thus, we performed gene profiling of hESC maintained under normoxic or hypoxic (1% or 5% O(2)) conditions. Our analysis revealed that hypoxia downregulates expression of pluripotency markers in hESC but increases significantly the expression of genes associated with angio- and vasculogenesis including vascular endothelial growth factor and angiopoitein-like proteins. Consequently, we were able to efficiently differentiate hESC to functional endothelial cells (EC) by varying O(2) levels; after 24 hours at 5% O(2), more than 50% of cells were CD34+. Transplantation of resulting endothelial-like cells improved both systolic function and fractional shortening in a rodent model of myocardial infarction. Moreover, analysis of the infarcted zone revealed that transplanted EC reduced the area of fibrous scar tissue by 50%. Thus, use of hypoxic conditions to specify the endothelial lineage suggests a novel strategy for cellular therapies aimed at repair of damaged vasculature in pathologies such as cerebral ischemia and myocardial infarction.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/20049902?dopt=Abstract</style></custom1></record></records></xml>