The Experts below are selected from a list of 285 Experts worldwide ranked by ideXlab platform
Elena Cano - One of the best experts on this subject based on the ideXlab platform.
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conditional deletion of wt1 in the Septum Transversum mesenchyme causes congenital diaphragmatic hernia in mice
eLife, 2016Co-Authors: Rita Carmona, Elena Cano, Anabel Rojas, Ana Canete, Laura Ariza, Ramon MunozchapuliAbstract:Congenital diaphragmatic hernia (CDH) is a severe birth defect. Wt1-null mouse embryos develop CDH but the mechanisms regulated by WT1 are unknown. We have generated a murine model with conditional deletion of WT1 in the lateral plate mesoderm, using the G2 enhancer of the Gata4 gene as a driver. 80% of G2-Gata4Cre;Wt1fl/fl embryos developed typical Bochdalek-type CDH. We show that the posthepatic mesenchymal plate coelomic epithelium gives rise to a mesenchyme that populates the pleuroperitoneal folds isolating the pleural cavities before the migration of the somitic myoblasts. This process fails when Wt1 is deleted from this area. Mutant embryos show Raldh2 downregulation in the lateral mesoderm, but not in the intermediate mesoderm. The mutant phenotype was partially rescued by retinoic acid treatment of the pregnant females. Replacement of intermediate by lateral mesoderm recapitulates the evolutionary origin of the diaphragm in mammals. CDH might thus be viewed as an evolutionary atavism.
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extracardiac Septum Transversum proepicardial endothelial cells pattern embryonic coronary arterio venous connections
Proceedings of the National Academy of Sciences of the United States of America, 2016Co-Authors: Elena Cano, Rita Carmona, Adrian Ruizvillalba, Anabel Rojas, Youying Chau, Kay D Wagner, Nicole WagnerAbstract:Recent reports suggest that mammalian embryonic coronary endothelium (CoE) originates from the sinus venosus and ventricular endocardium. However, the contribution of extracardiac cells to CoE is thought to be minor and nonsignificant for coronary formation. Using classic (Wt1Cre) and previously undescribed (G2-Gata4Cre) transgenic mouse models for the study of coronary vascular development, we show that extracardiac Septum Transversum/proepicardium (ST/PE)-derived endothelial cells are required for the formation of ventricular coronary arterio–venous vascular connections. Our results indicate that at least 20% of embryonic coronary arterial and capillary endothelial cells derive from the ST/PE compartment. Moreover, we show that conditional deletion of the ST/PE lineage-specific Wilms’ tumor suppressor gene (Wt1) in the ST/PE ofG2-Gata4Cre mice and in the endothelium of Tie2Cre mice disrupts embryonic coronary transmural patterning, leading to embryonic death. Taken together, our results demonstrate that ST/PE-derived endothelial cells contribute significantly to and are required for proper coronary vascular morphogenesis.
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Extracardiac Septum Transversum/proepicardial endothelial cells pattern embryonic coronary arterio-venous connections
Proceedings of the National Academy of Sciences of the United States of America, 2016Co-Authors: Elena Cano, Rita Carmona, Anabel Rojas, Youying Chau, Kay D Wagner, Nicole Wagner, Adrián Ruiz-villalba, Nicholas D. Hastie, Ramón Muñoz-chápuli, José M. Pérez-pomaresAbstract:Recent reports suggest that mammalian embryonic coronary endothelium (CoE) originates from the sinus venosus and ventricular endocardium. However, the contribution of extracardiac cells to CoE is thought to be minor and nonsignificant for coronary formation. Using classic (Wt1Cre) and previously undescribed (G2-Gata4Cre) transgenic mouse models for the study of coronary vascular development, we show that extracardiac Septum Transversum/proepicardium (ST/PE)-derived endothelial cells are required for the formation of ventricular coronary arterio–venous vascular connections. Our results indicate that at least 20% of embryonic coronary arterial and capillary endothelial cells derive from the ST/PE compartment. Moreover, we show that conditional deletion of the ST/PE lineage-specific Wilms’ tumor suppressor gene (Wt1) in the ST/PE ofG2-Gata4Cre mice and in the endothelium of Tie2Cre mice disrupts embryonic coronary transmural patterning, leading to embryonic death. Taken together, our results demonstrate that ST/PE-derived endothelial cells contribute significantly to and are required for proper coronary vascular morphogenesis.
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gata4 loss in the Septum Transversum mesenchyme promotes liver fibrosis in mice
Hepatology, 2014Co-Authors: Irene Delgado, Manuel Carrasco, Elena Cano, Rita Carmona, R Garciacarbonero, Luis Miguel Maringomez, Bernat Soria, Francisco Martin, David A Cano, Ramon MunozchapuliAbstract:The zinc finger transcription factor GATA4 controls specification and differentiation of multiple cell types during embryonic development. In mouse embryonic liver, Gata4 is expressed in the endodermal hepatic bud and in the adjacent mesenchyme of the Septum Transversum. Previous studies have shown that Gata4 inactivation impairs liver formation. However, whether these defects are caused by loss of Gata4 in the hepatic endoderm or in the Septum Transversum mesenchyme remains to be determined. In this study, we have investigated the role of mesenchymal GATA4 activity in liver formation. We have conditionally inactivated Gata4 in the Septum Transversum mesenchyme and its derivatives by using Cre/loxP technology. We have generated a mouse transgenic Cre line, in which expression of Cre recombinase is controlled by a previously identified distal Gata4 enhancer. Conditional inactivation of Gata4 in hepatic mesenchymal cells led to embryonic lethality around mouse embryonic stage 13.5, likely as a consequence of fetal anemia. Gata4 knockout fetal livers exhibited reduced size, advanced fibrosis, accumulation of extracellular matrix components and hepatic stellate cell (HSC) activation. Haploinsufficiency of Gata4 accelerated CCl4-induced liver fibrosis in adult mice. Moreover, Gata4 expression was dramatically reduced in advanced hepatic fibrosis and cirrhosis in humans. Conclusions: Our data demonstrate that mesenchymal GATA4 activity regulates HSC activation and inhibits the liver fibrogenic process. (Hepatology 2014;59:2358–2370)
Rita Carmona - One of the best experts on this subject based on the ideXlab platform.
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conditional deletion of wt1 in the Septum Transversum mesenchyme causes congenital diaphragmatic hernia in mice
eLife, 2016Co-Authors: Rita Carmona, Elena Cano, Anabel Rojas, Ana Canete, Laura Ariza, Ramon MunozchapuliAbstract:Congenital diaphragmatic hernia (CDH) is a severe birth defect. Wt1-null mouse embryos develop CDH but the mechanisms regulated by WT1 are unknown. We have generated a murine model with conditional deletion of WT1 in the lateral plate mesoderm, using the G2 enhancer of the Gata4 gene as a driver. 80% of G2-Gata4Cre;Wt1fl/fl embryos developed typical Bochdalek-type CDH. We show that the posthepatic mesenchymal plate coelomic epithelium gives rise to a mesenchyme that populates the pleuroperitoneal folds isolating the pleural cavities before the migration of the somitic myoblasts. This process fails when Wt1 is deleted from this area. Mutant embryos show Raldh2 downregulation in the lateral mesoderm, but not in the intermediate mesoderm. The mutant phenotype was partially rescued by retinoic acid treatment of the pregnant females. Replacement of intermediate by lateral mesoderm recapitulates the evolutionary origin of the diaphragm in mammals. CDH might thus be viewed as an evolutionary atavism.
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extracardiac Septum Transversum proepicardial endothelial cells pattern embryonic coronary arterio venous connections
Proceedings of the National Academy of Sciences of the United States of America, 2016Co-Authors: Elena Cano, Rita Carmona, Adrian Ruizvillalba, Anabel Rojas, Youying Chau, Kay D Wagner, Nicole WagnerAbstract:Recent reports suggest that mammalian embryonic coronary endothelium (CoE) originates from the sinus venosus and ventricular endocardium. However, the contribution of extracardiac cells to CoE is thought to be minor and nonsignificant for coronary formation. Using classic (Wt1Cre) and previously undescribed (G2-Gata4Cre) transgenic mouse models for the study of coronary vascular development, we show that extracardiac Septum Transversum/proepicardium (ST/PE)-derived endothelial cells are required for the formation of ventricular coronary arterio–venous vascular connections. Our results indicate that at least 20% of embryonic coronary arterial and capillary endothelial cells derive from the ST/PE compartment. Moreover, we show that conditional deletion of the ST/PE lineage-specific Wilms’ tumor suppressor gene (Wt1) in the ST/PE ofG2-Gata4Cre mice and in the endothelium of Tie2Cre mice disrupts embryonic coronary transmural patterning, leading to embryonic death. Taken together, our results demonstrate that ST/PE-derived endothelial cells contribute significantly to and are required for proper coronary vascular morphogenesis.
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Extracardiac Septum Transversum/proepicardial endothelial cells pattern embryonic coronary arterio-venous connections
Proceedings of the National Academy of Sciences of the United States of America, 2016Co-Authors: Elena Cano, Rita Carmona, Anabel Rojas, Youying Chau, Kay D Wagner, Nicole Wagner, Adrián Ruiz-villalba, Nicholas D. Hastie, Ramón Muñoz-chápuli, José M. Pérez-pomaresAbstract:Recent reports suggest that mammalian embryonic coronary endothelium (CoE) originates from the sinus venosus and ventricular endocardium. However, the contribution of extracardiac cells to CoE is thought to be minor and nonsignificant for coronary formation. Using classic (Wt1Cre) and previously undescribed (G2-Gata4Cre) transgenic mouse models for the study of coronary vascular development, we show that extracardiac Septum Transversum/proepicardium (ST/PE)-derived endothelial cells are required for the formation of ventricular coronary arterio–venous vascular connections. Our results indicate that at least 20% of embryonic coronary arterial and capillary endothelial cells derive from the ST/PE compartment. Moreover, we show that conditional deletion of the ST/PE lineage-specific Wilms’ tumor suppressor gene (Wt1) in the ST/PE ofG2-Gata4Cre mice and in the endothelium of Tie2Cre mice disrupts embryonic coronary transmural patterning, leading to embryonic death. Taken together, our results demonstrate that ST/PE-derived endothelial cells contribute significantly to and are required for proper coronary vascular morphogenesis.
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gata4 loss in the Septum Transversum mesenchyme promotes liver fibrosis in mice
Hepatology, 2014Co-Authors: Irene Delgado, Manuel Carrasco, Elena Cano, Rita Carmona, R Garciacarbonero, Luis Miguel Maringomez, Bernat Soria, Francisco Martin, David A Cano, Ramon MunozchapuliAbstract:The zinc finger transcription factor GATA4 controls specification and differentiation of multiple cell types during embryonic development. In mouse embryonic liver, Gata4 is expressed in the endodermal hepatic bud and in the adjacent mesenchyme of the Septum Transversum. Previous studies have shown that Gata4 inactivation impairs liver formation. However, whether these defects are caused by loss of Gata4 in the hepatic endoderm or in the Septum Transversum mesenchyme remains to be determined. In this study, we have investigated the role of mesenchymal GATA4 activity in liver formation. We have conditionally inactivated Gata4 in the Septum Transversum mesenchyme and its derivatives by using Cre/loxP technology. We have generated a mouse transgenic Cre line, in which expression of Cre recombinase is controlled by a previously identified distal Gata4 enhancer. Conditional inactivation of Gata4 in hepatic mesenchymal cells led to embryonic lethality around mouse embryonic stage 13.5, likely as a consequence of fetal anemia. Gata4 knockout fetal livers exhibited reduced size, advanced fibrosis, accumulation of extracellular matrix components and hepatic stellate cell (HSC) activation. Haploinsufficiency of Gata4 accelerated CCl4-induced liver fibrosis in adult mice. Moreover, Gata4 expression was dramatically reduced in advanced hepatic fibrosis and cirrhosis in humans. Conclusions: Our data demonstrate that mesenchymal GATA4 activity regulates HSC activation and inhibits the liver fibrogenic process. (Hepatology 2014;59:2358–2370)
Nicole Wagner - One of the best experts on this subject based on the ideXlab platform.
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extracardiac Septum Transversum proepicardial endothelial cells pattern embryonic coronary arterio venous connections
Proceedings of the National Academy of Sciences of the United States of America, 2016Co-Authors: Elena Cano, Rita Carmona, Adrian Ruizvillalba, Anabel Rojas, Youying Chau, Kay D Wagner, Nicole WagnerAbstract:Recent reports suggest that mammalian embryonic coronary endothelium (CoE) originates from the sinus venosus and ventricular endocardium. However, the contribution of extracardiac cells to CoE is thought to be minor and nonsignificant for coronary formation. Using classic (Wt1Cre) and previously undescribed (G2-Gata4Cre) transgenic mouse models for the study of coronary vascular development, we show that extracardiac Septum Transversum/proepicardium (ST/PE)-derived endothelial cells are required for the formation of ventricular coronary arterio–venous vascular connections. Our results indicate that at least 20% of embryonic coronary arterial and capillary endothelial cells derive from the ST/PE compartment. Moreover, we show that conditional deletion of the ST/PE lineage-specific Wilms’ tumor suppressor gene (Wt1) in the ST/PE ofG2-Gata4Cre mice and in the endothelium of Tie2Cre mice disrupts embryonic coronary transmural patterning, leading to embryonic death. Taken together, our results demonstrate that ST/PE-derived endothelial cells contribute significantly to and are required for proper coronary vascular morphogenesis.
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Extracardiac Septum Transversum/proepicardial endothelial cells pattern embryonic coronary arterio-venous connections
Proceedings of the National Academy of Sciences of the United States of America, 2016Co-Authors: Elena Cano, Rita Carmona, Anabel Rojas, Youying Chau, Kay D Wagner, Nicole Wagner, Adrián Ruiz-villalba, Nicholas D. Hastie, Ramón Muñoz-chápuli, José M. Pérez-pomaresAbstract:Recent reports suggest that mammalian embryonic coronary endothelium (CoE) originates from the sinus venosus and ventricular endocardium. However, the contribution of extracardiac cells to CoE is thought to be minor and nonsignificant for coronary formation. Using classic (Wt1Cre) and previously undescribed (G2-Gata4Cre) transgenic mouse models for the study of coronary vascular development, we show that extracardiac Septum Transversum/proepicardium (ST/PE)-derived endothelial cells are required for the formation of ventricular coronary arterio–venous vascular connections. Our results indicate that at least 20% of embryonic coronary arterial and capillary endothelial cells derive from the ST/PE compartment. Moreover, we show that conditional deletion of the ST/PE lineage-specific Wilms’ tumor suppressor gene (Wt1) in the ST/PE ofG2-Gata4Cre mice and in the endothelium of Tie2Cre mice disrupts embryonic coronary transmural patterning, leading to embryonic death. Taken together, our results demonstrate that ST/PE-derived endothelial cells contribute significantly to and are required for proper coronary vascular morphogenesis.
Youying Chau - One of the best experts on this subject based on the ideXlab platform.
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extracardiac Septum Transversum proepicardial endothelial cells pattern embryonic coronary arterio venous connections
Proceedings of the National Academy of Sciences of the United States of America, 2016Co-Authors: Elena Cano, Rita Carmona, Adrian Ruizvillalba, Anabel Rojas, Youying Chau, Kay D Wagner, Nicole WagnerAbstract:Recent reports suggest that mammalian embryonic coronary endothelium (CoE) originates from the sinus venosus and ventricular endocardium. However, the contribution of extracardiac cells to CoE is thought to be minor and nonsignificant for coronary formation. Using classic (Wt1Cre) and previously undescribed (G2-Gata4Cre) transgenic mouse models for the study of coronary vascular development, we show that extracardiac Septum Transversum/proepicardium (ST/PE)-derived endothelial cells are required for the formation of ventricular coronary arterio–venous vascular connections. Our results indicate that at least 20% of embryonic coronary arterial and capillary endothelial cells derive from the ST/PE compartment. Moreover, we show that conditional deletion of the ST/PE lineage-specific Wilms’ tumor suppressor gene (Wt1) in the ST/PE ofG2-Gata4Cre mice and in the endothelium of Tie2Cre mice disrupts embryonic coronary transmural patterning, leading to embryonic death. Taken together, our results demonstrate that ST/PE-derived endothelial cells contribute significantly to and are required for proper coronary vascular morphogenesis.
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Extracardiac Septum Transversum/proepicardial endothelial cells pattern embryonic coronary arterio-venous connections
Proceedings of the National Academy of Sciences of the United States of America, 2016Co-Authors: Elena Cano, Rita Carmona, Anabel Rojas, Youying Chau, Kay D Wagner, Nicole Wagner, Adrián Ruiz-villalba, Nicholas D. Hastie, Ramón Muñoz-chápuli, José M. Pérez-pomaresAbstract:Recent reports suggest that mammalian embryonic coronary endothelium (CoE) originates from the sinus venosus and ventricular endocardium. However, the contribution of extracardiac cells to CoE is thought to be minor and nonsignificant for coronary formation. Using classic (Wt1Cre) and previously undescribed (G2-Gata4Cre) transgenic mouse models for the study of coronary vascular development, we show that extracardiac Septum Transversum/proepicardium (ST/PE)-derived endothelial cells are required for the formation of ventricular coronary arterio–venous vascular connections. Our results indicate that at least 20% of embryonic coronary arterial and capillary endothelial cells derive from the ST/PE compartment. Moreover, we show that conditional deletion of the ST/PE lineage-specific Wilms’ tumor suppressor gene (Wt1) in the ST/PE ofG2-Gata4Cre mice and in the endothelium of Tie2Cre mice disrupts embryonic coronary transmural patterning, leading to embryonic death. Taken together, our results demonstrate that ST/PE-derived endothelial cells contribute significantly to and are required for proper coronary vascular morphogenesis.
Anabel Rojas - One of the best experts on this subject based on the ideXlab platform.
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coup tfii expression defines two different Septum Transversum cell compartments crucial to cardiac septation and compact ventricular wall growth
2018Co-Authors: Juan Antonio Guadix, Anabel Rojas, Adriana Piresgomes, Sara Cano, Cristina Pogontke, Paul Palmquistgomes, Jose M PerezpomaresAbstract:Universidad de Malaga. Campus de Excelencia Internacional Andalucia Tech. Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII)
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conditional deletion of wt1 in the Septum Transversum mesenchyme causes congenital diaphragmatic hernia in mice
eLife, 2016Co-Authors: Rita Carmona, Elena Cano, Anabel Rojas, Ana Canete, Laura Ariza, Ramon MunozchapuliAbstract:Congenital diaphragmatic hernia (CDH) is a severe birth defect. Wt1-null mouse embryos develop CDH but the mechanisms regulated by WT1 are unknown. We have generated a murine model with conditional deletion of WT1 in the lateral plate mesoderm, using the G2 enhancer of the Gata4 gene as a driver. 80% of G2-Gata4Cre;Wt1fl/fl embryos developed typical Bochdalek-type CDH. We show that the posthepatic mesenchymal plate coelomic epithelium gives rise to a mesenchyme that populates the pleuroperitoneal folds isolating the pleural cavities before the migration of the somitic myoblasts. This process fails when Wt1 is deleted from this area. Mutant embryos show Raldh2 downregulation in the lateral mesoderm, but not in the intermediate mesoderm. The mutant phenotype was partially rescued by retinoic acid treatment of the pregnant females. Replacement of intermediate by lateral mesoderm recapitulates the evolutionary origin of the diaphragm in mammals. CDH might thus be viewed as an evolutionary atavism.
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extracardiac Septum Transversum proepicardial endothelial cells pattern embryonic coronary arterio venous connections
Proceedings of the National Academy of Sciences of the United States of America, 2016Co-Authors: Elena Cano, Rita Carmona, Adrian Ruizvillalba, Anabel Rojas, Youying Chau, Kay D Wagner, Nicole WagnerAbstract:Recent reports suggest that mammalian embryonic coronary endothelium (CoE) originates from the sinus venosus and ventricular endocardium. However, the contribution of extracardiac cells to CoE is thought to be minor and nonsignificant for coronary formation. Using classic (Wt1Cre) and previously undescribed (G2-Gata4Cre) transgenic mouse models for the study of coronary vascular development, we show that extracardiac Septum Transversum/proepicardium (ST/PE)-derived endothelial cells are required for the formation of ventricular coronary arterio–venous vascular connections. Our results indicate that at least 20% of embryonic coronary arterial and capillary endothelial cells derive from the ST/PE compartment. Moreover, we show that conditional deletion of the ST/PE lineage-specific Wilms’ tumor suppressor gene (Wt1) in the ST/PE ofG2-Gata4Cre mice and in the endothelium of Tie2Cre mice disrupts embryonic coronary transmural patterning, leading to embryonic death. Taken together, our results demonstrate that ST/PE-derived endothelial cells contribute significantly to and are required for proper coronary vascular morphogenesis.
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Extracardiac Septum Transversum/proepicardial endothelial cells pattern embryonic coronary arterio-venous connections
Proceedings of the National Academy of Sciences of the United States of America, 2016Co-Authors: Elena Cano, Rita Carmona, Anabel Rojas, Youying Chau, Kay D Wagner, Nicole Wagner, Adrián Ruiz-villalba, Nicholas D. Hastie, Ramón Muñoz-chápuli, José M. Pérez-pomaresAbstract:Recent reports suggest that mammalian embryonic coronary endothelium (CoE) originates from the sinus venosus and ventricular endocardium. However, the contribution of extracardiac cells to CoE is thought to be minor and nonsignificant for coronary formation. Using classic (Wt1Cre) and previously undescribed (G2-Gata4Cre) transgenic mouse models for the study of coronary vascular development, we show that extracardiac Septum Transversum/proepicardium (ST/PE)-derived endothelial cells are required for the formation of ventricular coronary arterio–venous vascular connections. Our results indicate that at least 20% of embryonic coronary arterial and capillary endothelial cells derive from the ST/PE compartment. Moreover, we show that conditional deletion of the ST/PE lineage-specific Wilms’ tumor suppressor gene (Wt1) in the ST/PE ofG2-Gata4Cre mice and in the endothelium of Tie2Cre mice disrupts embryonic coronary transmural patterning, leading to embryonic death. Taken together, our results demonstrate that ST/PE-derived endothelial cells contribute significantly to and are required for proper coronary vascular morphogenesis.
