conditional ablation of ezh2 in murine hearts reveals its essential roles in endocardial cushion formation, cardiomyocyte proliferation and survival条件消融ezh2的小鼠心脏心内膜垫形成显示其重要作用,心肌细胞增殖和生存.pdfVIP

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2017-09-12 发布于上海
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conditional ablation of ezh2 in murine hearts reveals its essential roles in endocardial cushion formation, cardiomyocyte proliferation and survival条件消融ezh2的小鼠心脏心内膜垫形成显示其重要作用,心肌细胞增殖和生存.pdf

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conditional ablation of ezh2 in murine hearts reveals its essential roles in endocardial cushion formation, cardiomyocyte proliferation and survival条件消融ezh2的小鼠心脏心内膜垫形成显示其重要作用,心肌细胞增殖和生存

Conditional Ablation of Ezh2 in Murine Hearts Reveals Its Essential Roles in Endocardial Cushion Formation, Cardiomyocyte Proliferation and Survival 1 2 1,3 4 4 1 1 Li Chen , Yanlin Ma , Eun Young Kim , Wei Yu , Robert J. Schwartz , Ling Qian , Jun Wang * 1 Department of Stem Cell Engineering, Basic Research Laboratories, Texas Heart Institute, Houston, Texas, United States of America, 2 Institute of Biosciences and Technology, Texas AM Health Science Center, Houston, Texas, United States of America, 3 Program in Genes and Development, The University of Texas Health Science Center at Houston, Houston, Texas, United States of America, 4 Department of Biochemistry and Molecular Biology, University of Houston, Houston, Texas, United States of America Abstract Ezh2 is a histone trimethyltransferase that silences genes mainly via catalyzing trimethylation of histone 3 lysine 27 (H3K27Me3). The role of Ezh2 as a regulator of gene silencing and cell proliferation in cancer development has been extensively investigated; however, its function in heart development during embryonic cardiogenesis has not been well studied. In the present study, we used a genetically modified mouse system in which Ezh2 was specifically ablated in the mouse heart. We identified a wide spectrum of cardiovascular malformations in the Ezh2 mutant mice, which collectively led to perinatal death. In the Ezh2 mutant heart, the endocardial cushions (ECs) were hypoplastic and the endothelial-to- mesenchymal transition (EMT) process was impaired. The hearts of Ezh2 mutant mice also exhibited decreased cardiomyocyte proliferation and increased apoptosis. We