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Rie Saba - One of the best experts on this subject based on the ideXlab platform.
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endocardium differentiation through sox17 expression in endocardium precursor cells regulates Heart Development in mice
2019Co-Authors: Rie Saba, Keiko Kitajima, Lucille Rainbow, Sylvia Engert, Mami Uemura, Hidekazu Ishida, Ioannis KokkinopoulosAbstract:The endocardium is the endothelial component of the vertebrate Heart and plays a key role in Heart Development. Where, when, and how the endocardium segregates during embryogenesis have remained largely unknown, however. We now show that Nkx2-5+ cardiac progenitor cells (CPCs) that express the Sry-type HMG box gene Sox17 from embryonic day (E) 7.5 to E8.5 specifically differentiate into the endocardium in mouse embryos. Although Sox17 is not essential or sufficient for endocardium fate, it can bias the fate of CPCs toward the endocardium. On the other hand, Sox17 expression in the endocardium is required for Heart Development. Deletion of Sox17 specifically in the mesoderm markedly impaired endocardium Development with regard to cell proliferation and behavior. The proliferation of cardiomyocytes, ventricular trabeculation, and myocardium thickening were also impaired in a non-cell-autonomous manner in the Sox17 mutant, likely as a consequence of down-regulation of NOTCH signaling. An unknown signal, regulated by Sox17 and required for nurturing of the myocardium, is responsible for the reduction in NOTCH-related genes in the mutant embryos. Our results thus provide insight into differentiation of the endocardium and its role in Heart Development.
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sox17 expression in endocardium precursor cells regulates Heart Development in mice
2019Co-Authors: Rie Saba, Keiko Kitajima, Lucille Rainbow, Sylvia Engert, Mami Uemura, Hidekazu Ishida, Ioannis Kokkinopoulos, Yasunori Shintani, Shigeru MiyagawaAbstract:The endocardium is the endothelial component of the vertebrate Heart and plays a key role in Heart Development. Cardiac progenitor cells (CPCs) that express the homeobox gene Nkx2-5 give rise to the endocardium. Where, when, and how the endocardium segregates during embryogenesis have remained largely unknown, however. We now show that Nkx2-5+ CPCs that express the Sry-type HMG box gene Sox17 specifically differentiate into the endocardium in mouse embryos. Approximately 20% to 30% of Nkx2-5+ CPCs transiently express Sox17 from embryonic day (E) 7.5 to E8.5. Although Sox17 is not essential or sufficient for endocardium fate, it can bias the fate of CPCs toward the endocardium. On the other hand, Sox17 expression in the endocardium is required for Heart Development. Deletion of Sox17 specifically in the mesoderm markedly impaired endocardium Development with regard to cell proliferation and behavior. The proliferation of cardiomyocytes, ventricular trabeculation, and myocardium thickening were also impaired in a non-cell-autonomous manner in the Sox17 mutant, resulting in anomalous morphology of the Heart, likely as a consequence of down-regulation of NOTCH signaling. Changes in gene expression profile in both the endocardium and myocardium preceded the reduction in NOTCH-related gene expression in the mutant embryos, suggesting that Sox17 expression in the endocardium regulates an unknown signal required for nurturing of the myocardium. Our results thus provide insight into differentiation of the endocardium and its role in Heart Development.
Mami Uemura - One of the best experts on this subject based on the ideXlab platform.
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endocardium differentiation through sox17 expression in endocardium precursor cells regulates Heart Development in mice
2019Co-Authors: Rie Saba, Keiko Kitajima, Lucille Rainbow, Sylvia Engert, Mami Uemura, Hidekazu Ishida, Ioannis KokkinopoulosAbstract:The endocardium is the endothelial component of the vertebrate Heart and plays a key role in Heart Development. Where, when, and how the endocardium segregates during embryogenesis have remained largely unknown, however. We now show that Nkx2-5+ cardiac progenitor cells (CPCs) that express the Sry-type HMG box gene Sox17 from embryonic day (E) 7.5 to E8.5 specifically differentiate into the endocardium in mouse embryos. Although Sox17 is not essential or sufficient for endocardium fate, it can bias the fate of CPCs toward the endocardium. On the other hand, Sox17 expression in the endocardium is required for Heart Development. Deletion of Sox17 specifically in the mesoderm markedly impaired endocardium Development with regard to cell proliferation and behavior. The proliferation of cardiomyocytes, ventricular trabeculation, and myocardium thickening were also impaired in a non-cell-autonomous manner in the Sox17 mutant, likely as a consequence of down-regulation of NOTCH signaling. An unknown signal, regulated by Sox17 and required for nurturing of the myocardium, is responsible for the reduction in NOTCH-related genes in the mutant embryos. Our results thus provide insight into differentiation of the endocardium and its role in Heart Development.
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sox17 expression in endocardium precursor cells regulates Heart Development in mice
2019Co-Authors: Rie Saba, Keiko Kitajima, Lucille Rainbow, Sylvia Engert, Mami Uemura, Hidekazu Ishida, Ioannis Kokkinopoulos, Yasunori Shintani, Shigeru MiyagawaAbstract:The endocardium is the endothelial component of the vertebrate Heart and plays a key role in Heart Development. Cardiac progenitor cells (CPCs) that express the homeobox gene Nkx2-5 give rise to the endocardium. Where, when, and how the endocardium segregates during embryogenesis have remained largely unknown, however. We now show that Nkx2-5+ CPCs that express the Sry-type HMG box gene Sox17 specifically differentiate into the endocardium in mouse embryos. Approximately 20% to 30% of Nkx2-5+ CPCs transiently express Sox17 from embryonic day (E) 7.5 to E8.5. Although Sox17 is not essential or sufficient for endocardium fate, it can bias the fate of CPCs toward the endocardium. On the other hand, Sox17 expression in the endocardium is required for Heart Development. Deletion of Sox17 specifically in the mesoderm markedly impaired endocardium Development with regard to cell proliferation and behavior. The proliferation of cardiomyocytes, ventricular trabeculation, and myocardium thickening were also impaired in a non-cell-autonomous manner in the Sox17 mutant, resulting in anomalous morphology of the Heart, likely as a consequence of down-regulation of NOTCH signaling. Changes in gene expression profile in both the endocardium and myocardium preceded the reduction in NOTCH-related gene expression in the mutant embryos, suggesting that Sox17 expression in the endocardium regulates an unknown signal required for nurturing of the myocardium. Our results thus provide insight into differentiation of the endocardium and its role in Heart Development.
Ioannis Kokkinopoulos - One of the best experts on this subject based on the ideXlab platform.
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endocardium differentiation through sox17 expression in endocardium precursor cells regulates Heart Development in mice
2019Co-Authors: Rie Saba, Keiko Kitajima, Lucille Rainbow, Sylvia Engert, Mami Uemura, Hidekazu Ishida, Ioannis KokkinopoulosAbstract:The endocardium is the endothelial component of the vertebrate Heart and plays a key role in Heart Development. Where, when, and how the endocardium segregates during embryogenesis have remained largely unknown, however. We now show that Nkx2-5+ cardiac progenitor cells (CPCs) that express the Sry-type HMG box gene Sox17 from embryonic day (E) 7.5 to E8.5 specifically differentiate into the endocardium in mouse embryos. Although Sox17 is not essential or sufficient for endocardium fate, it can bias the fate of CPCs toward the endocardium. On the other hand, Sox17 expression in the endocardium is required for Heart Development. Deletion of Sox17 specifically in the mesoderm markedly impaired endocardium Development with regard to cell proliferation and behavior. The proliferation of cardiomyocytes, ventricular trabeculation, and myocardium thickening were also impaired in a non-cell-autonomous manner in the Sox17 mutant, likely as a consequence of down-regulation of NOTCH signaling. An unknown signal, regulated by Sox17 and required for nurturing of the myocardium, is responsible for the reduction in NOTCH-related genes in the mutant embryos. Our results thus provide insight into differentiation of the endocardium and its role in Heart Development.
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sox17 expression in endocardium precursor cells regulates Heart Development in mice
2019Co-Authors: Rie Saba, Keiko Kitajima, Lucille Rainbow, Sylvia Engert, Mami Uemura, Hidekazu Ishida, Ioannis Kokkinopoulos, Yasunori Shintani, Shigeru MiyagawaAbstract:The endocardium is the endothelial component of the vertebrate Heart and plays a key role in Heart Development. Cardiac progenitor cells (CPCs) that express the homeobox gene Nkx2-5 give rise to the endocardium. Where, when, and how the endocardium segregates during embryogenesis have remained largely unknown, however. We now show that Nkx2-5+ CPCs that express the Sry-type HMG box gene Sox17 specifically differentiate into the endocardium in mouse embryos. Approximately 20% to 30% of Nkx2-5+ CPCs transiently express Sox17 from embryonic day (E) 7.5 to E8.5. Although Sox17 is not essential or sufficient for endocardium fate, it can bias the fate of CPCs toward the endocardium. On the other hand, Sox17 expression in the endocardium is required for Heart Development. Deletion of Sox17 specifically in the mesoderm markedly impaired endocardium Development with regard to cell proliferation and behavior. The proliferation of cardiomyocytes, ventricular trabeculation, and myocardium thickening were also impaired in a non-cell-autonomous manner in the Sox17 mutant, resulting in anomalous morphology of the Heart, likely as a consequence of down-regulation of NOTCH signaling. Changes in gene expression profile in both the endocardium and myocardium preceded the reduction in NOTCH-related gene expression in the mutant embryos, suggesting that Sox17 expression in the endocardium regulates an unknown signal required for nurturing of the myocardium. Our results thus provide insight into differentiation of the endocardium and its role in Heart Development.
Hidekazu Ishida - One of the best experts on this subject based on the ideXlab platform.
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endocardium differentiation through sox17 expression in endocardium precursor cells regulates Heart Development in mice
2019Co-Authors: Rie Saba, Keiko Kitajima, Lucille Rainbow, Sylvia Engert, Mami Uemura, Hidekazu Ishida, Ioannis KokkinopoulosAbstract:The endocardium is the endothelial component of the vertebrate Heart and plays a key role in Heart Development. Where, when, and how the endocardium segregates during embryogenesis have remained largely unknown, however. We now show that Nkx2-5+ cardiac progenitor cells (CPCs) that express the Sry-type HMG box gene Sox17 from embryonic day (E) 7.5 to E8.5 specifically differentiate into the endocardium in mouse embryos. Although Sox17 is not essential or sufficient for endocardium fate, it can bias the fate of CPCs toward the endocardium. On the other hand, Sox17 expression in the endocardium is required for Heart Development. Deletion of Sox17 specifically in the mesoderm markedly impaired endocardium Development with regard to cell proliferation and behavior. The proliferation of cardiomyocytes, ventricular trabeculation, and myocardium thickening were also impaired in a non-cell-autonomous manner in the Sox17 mutant, likely as a consequence of down-regulation of NOTCH signaling. An unknown signal, regulated by Sox17 and required for nurturing of the myocardium, is responsible for the reduction in NOTCH-related genes in the mutant embryos. Our results thus provide insight into differentiation of the endocardium and its role in Heart Development.
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sox17 expression in endocardium precursor cells regulates Heart Development in mice
2019Co-Authors: Rie Saba, Keiko Kitajima, Lucille Rainbow, Sylvia Engert, Mami Uemura, Hidekazu Ishida, Ioannis Kokkinopoulos, Yasunori Shintani, Shigeru MiyagawaAbstract:The endocardium is the endothelial component of the vertebrate Heart and plays a key role in Heart Development. Cardiac progenitor cells (CPCs) that express the homeobox gene Nkx2-5 give rise to the endocardium. Where, when, and how the endocardium segregates during embryogenesis have remained largely unknown, however. We now show that Nkx2-5+ CPCs that express the Sry-type HMG box gene Sox17 specifically differentiate into the endocardium in mouse embryos. Approximately 20% to 30% of Nkx2-5+ CPCs transiently express Sox17 from embryonic day (E) 7.5 to E8.5. Although Sox17 is not essential or sufficient for endocardium fate, it can bias the fate of CPCs toward the endocardium. On the other hand, Sox17 expression in the endocardium is required for Heart Development. Deletion of Sox17 specifically in the mesoderm markedly impaired endocardium Development with regard to cell proliferation and behavior. The proliferation of cardiomyocytes, ventricular trabeculation, and myocardium thickening were also impaired in a non-cell-autonomous manner in the Sox17 mutant, resulting in anomalous morphology of the Heart, likely as a consequence of down-regulation of NOTCH signaling. Changes in gene expression profile in both the endocardium and myocardium preceded the reduction in NOTCH-related gene expression in the mutant embryos, suggesting that Sox17 expression in the endocardium regulates an unknown signal required for nurturing of the myocardium. Our results thus provide insight into differentiation of the endocardium and its role in Heart Development.
Wolfgang A Linke - One of the best experts on this subject based on the ideXlab platform.
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Plasticity of cardiac titin/connectin in Heart Development q
2013Co-Authors: Christiane A Opitz, Wolfgang A LinkeAbstract:Many sarcomeric proteins in the myocardium alter their isoform pattern during perinatal Development to adjust to the intensified pump function of the postnatal Heart. These changes also involve the giant protein titin/connectin. Here we show by low-percentage polyacrylamide-gel electrophoresis that Developmentally regulated switching of cardiac titin/connectin size occurs in the Hearts of mouse, rat, pig, and chicken. Mammalian Hearts express, well before birth, large foetal ( 3.7 MDa) N2BA-titin/connectin isoform but no N2B-isoform (3.0 MDa). During perinatal Heart Development the 3.7-MDa N2BA-isoform is replaced by a mix of smaller isoforms. At birth a plethora of intermediate-size N2BA-isoforms appears together with the N2B-isoform. In postnatal Heart Development the larger-size N2BA-isoforms disappear and smaller-size N2BA-isoforms are upregulated, whereas the proportion of N2B-titin/connectin increases to species-specific adult levels. The time courses of isoform switching are faster in small than in large mammals. Titin/connectin isoform switching also takes place in developing chicken Hearts, but the largest embryonic isoform found here was less than 3.4 MDa. At hatching, various smaller-size isoforms appeared and within a week the adult expression pattern was established representing a major 3.0-MDa isoform and a minor 3.15-MDa isoform. The ratio between the two adult isoforms differed between the left ventricle and the right atrium. The perinatal changes toward smaller cardiac titin/connectin isoforms in mammals and chicken greatly increase the myofibrillar passive tension of postnatal Hearts. Plasticity of titin/connectin at approximately the time of birth thus affects myocardial mechanics but could also be an important factor in Developmentally regulated assembly and signalling processes
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plasticity of cardiac titin connectin in Heart Development
2006Co-Authors: Christiane A Opitz, Wolfgang A LinkeAbstract:Many sarcomeric proteins in the myocardium alter their isoform pattern during perinatal Development to adjust to the intensified pump function of the postnatal Heart. These changes also involve the giant protein titin/connectin. Here we show by low-percentage polyacrylamide-gel electrophoresis that Developmentally regulated switching of cardiac titin/connectin size occurs in the Hearts of mouse, rat, pig, and chicken. Mammalian Hearts express, well before birth, large foetal (approximately 3.7 MDa) N2BA-titin/connectin isoform but no N2B-isoform (3.0 MDa). During perinatal Heart Development the 3.7-MDa N2BA-isoform is replaced by a mix of smaller isoforms. At birth a plethora of intermediate-size N2BA-isoforms appears together with the N2B-isoform. In postnatal Heart Development the larger-size N2BA-isoforms disappear and smaller-size N2BA-isoforms are upregulated, whereas the proportion of N2B-titin/connectin increases to species-specific adult levels. The time courses of isoform switching are faster in small than in large mammals. Titin/connectin isoform switching also takes place in developing chicken Hearts, but the largest embryonic isoform found here was less than 3.4 MDa. At hatching, various smaller-size isoforms appeared and within a week the adult expression pattern was established representing a major 3.0-MDa isoform and a minor 3.15-MDa isoform. The ratio between the two adult isoforms differed between the left ventricle and the right atrium. The perinatal changes toward smaller cardiac titin/connectin isoforms in mammals and chicken greatly increase the myofibrillar passive tension of postnatal Hearts. Plasticity of titin/connectin at approximately the time of birth thus affects myocardial mechanics but could also be an important factor in Developmentally regulated assembly and signalling processes.
