Myocardial Cellular Development and Morphogenesis

Zhu, Hong

doi:10.1016/b978-012436570-4/50004-2

Cited by 4 publications

(4 citation statements)

References 162 publications

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“…For example, the component term 'spliceosome' shows that 17 out of 20 genes (85%, z score of 6.7) were upregulated. The upregulation of these processes is consistent with the fact that cardiomyocytes remain mitotically active throughout embryonic development [ 17 ]. Apart from processes involved in cell division and growth, the MAPPFinder results indicate that the processes 'transmembrane receptor protein serine/threonine kinase signaling pathway' and 'induction of apoptosis' are upregulated, with a z score of approximately 2.…”

Section: Resultssupporting

confidence: 73%

“…The GO gene-association files [ 17 ] are potentially problematic, because they treat each GO term independently, removing the implicit parent-child relationship. As a result, looking at the GO terms individually is often uninformative because the number of genes associated with any one term is smaller than the actual number of genes involved in that process, component, or function.…”

Section: Methodsmentioning

confidence: 99%

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MAPPFinder: using Gene Ontology and GenMAPP to create a global gene-expression profile from microarray data

et al. 2003

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MAPPFinder is a tool that creates a global gene-expression profile across all areas of biology by integrating the annotations of the Gene Ontology (GO) Project with the free software package GenMAPP (http://www.GenMAPP.org). The results are displayed in a searchable browser, allowing the user to rapidly identify GO terms with over-represented numbers of geneexpression changes. Clicking on GO terms generates GenMAPP graphical files where gene relationships can be explored, annotated, and files can be freely exchanged. The electronic version of this article is the complete one and can be found online at

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Section: Resultssupporting

confidence: 73%

Section: Methodsmentioning

confidence: 99%

MAPPFinder: using Gene Ontology and GenMAPP to create a global gene-expression profile from microarray data

et al. 2003

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“…Mammalian cardiac and skeletal muscle are both derived from mesoderm and share many morphologic, physiologic, and biochemical properties [49]. However, one difference is that during embryonic development, cell proliferation and differentiation processes occur in skeletal muscle but not cardiac muscle [5].…”

Section: Introductionmentioning

confidence: 99%

“…However, one difference is that during embryonic development, cell proliferation and differentiation processes occur in skeletal muscle but not cardiac muscle [5]. In the developing embryo, committed skeletal muscle myoblasts proliferate until a certain cell mass has been reached and then start to fuse together, leading to permanent withdrawal from the cell cycle; that is, terminal differentiation [49]. In contrast, committed cardiac myoblasts differentiate into contractile cardiac muscle cells without withdrawing from the cell cycle.…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress-induced formation of a positive-feedback loop for the sustained activation of p38 MAPK leading to the loss of cell division in cardiomyocytes soon after birth

Matsuyama

Kikuchi

2011

Basic Res Cardiol

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Shortly after birth, mammalian cardiomyocytes irreversibly exit from the cell cycle and become terminally differentiated. The cellular mechanisms responsible for the cessation of cell division and terminal differentiation of cardiomyocytes soon after birth have intrigued developmental biologists as well as cardiovascular physicians, but the genetic cues for the irreversible exit from the cell cycle soon after birth remain largely unknown. We examined whether and if so how oxidative stress to mammalian hearts during fetal-neonatal transition produces changes in the proliferative activity and terminal differentiation of cardiomyocytes. Scavenging of reactive oxygen species (ROS) during fetal-neonatal transition, especially after birth, resulted in an increase in the proliferative activity and a decrease in the ratio of binucleated cardiomyocytes. Exposure to ROS in cultured cardiomyocytes increased the activity of p38 MAPK and the expression of connexin 43 (Cx43). Not only knockdown of Cx43 using siRNA but also the inhibition of p38 MAPK activity resulted in a significant decrease in the production of ROS in cardiomyocytes, suggesting that the signaling pathway ROS-p38 MAPK-Cx43 (especially, Cx43 at mitochondria, mtCx43) constituted a closed regulatory system with positive feedback. In addition, continuous scavenging of ROS or suppression of p38 MAPK activity for 4 days after birth resulted in a significant decrease in the expression of mtCx43 and in the number of binucleated cardiomyocytes. This study demonstrated that the ROS-induced formation of a positive-feedback loop ROS-p38 MAPK-mtCx43 for the sustained activation of p38 MAPK soon after birth possibly contributes to the loss of cell division and binucleation in mammalian cardiomyocytes.

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Phenylephrine protects neonatal rat cardiomyocytes from hypoxia and serum deprivation-induced apoptosis

et al. 2000

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Previous studies have shown that a-adrenergic activation reduces myocardial damages caused by ischemia/reperfusion. However, the molecular mechanisms of how a-adrenergic activation protects the myocardium are not completely understood. The objective of this study was to test the hypothesis that a-adrenergic activation protects the myocardium by, at least in part, inhibiting apoptosis in cardiomyocytes. The current data has shown that apoptosis in neonatal rat cardiomyocytes, induced by 24 h treatment with hypoxia (95% N 2 and 5% CO 2 ) and serum deprivation, was inhibited by co-treatment with phenylephrine. Pre-treatment with phenylephrine for 24 h also protected cardiomyocytes against subsequent 24 h treatment with hypoxia and serum deprivation. Exposure of cardiomyocytes to phenylephrine for up to 9 days under normoxic conditions did not cause apoptosis. The phenylephrinemediated cytoprotection was blocked by an a-adrenergic antagonist, phentolamine. b-adrenergic activation with isoproterenol did not protect cardiomyocytes against hypoxia and serum deprivation-induced apoptosis. Under hypoxic conditions,phenylephrinepreventedthedown-regulationofBcl-2and Bcl-X mRNA/protein and induced hypertrophic growth. Phenylephrine-mediated protection was abrogated by the phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor wortmannin and was mimicked by the caspase-9 peptidic inhibitor LEHD-fmk. These results suggest that a-adrenergic activation protects cardiomyocytes against hypoxia and serum deprivation-induced apoptosis through regulating the expression of mitochondrion-associated apoptosis regulatory genes, preventing activation of mitochondrial damage-induced apoptosis pathway (cytochrome C-caspase-9), and activating hypertrophic growth. Cell Death and Differentiation (2000) 7, 773 ± 784.

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Myocardial Cellular Development and Morphogenesis

Cited by 4 publications

References 162 publications

MAPPFinder: using Gene Ontology and GenMAPP to create a global gene-expression profile from microarray data

MAPPFinder: using Gene Ontology and GenMAPP to create a global gene-expression profile from microarray data

Oxidative stress-induced formation of a positive-feedback loop for the sustained activation of p38 MAPK leading to the loss of cell division in cardiomyocytes soon after birth

Phenylephrine protects neonatal rat cardiomyocytes from hypoxia and serum deprivation-induced apoptosis

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