The Experts below are selected from a list of 207 Experts worldwide ranked by ideXlab platform

Deborah Yelon - One of the best experts on this subject based on the ideXlab platform.

  • mutation of weak atrium Atrial Myosin heavy chain disrupts Atrial function and influences ventricular morphogenesis in zebrafish
    Development, 2003
    Co-Authors: Eli Berdougo, Hope Coleman, Diana H Lee, Didier Y R Stainier, Deborah Yelon
    Abstract:

    The embryonic vertebrate heart is composed of two major chambers, a ventricle and an atrium, each of which has a characteristic size, shape and functional capacity that contributes to efficient circulation. Chamber-specific gene expression programs are likely to regulate key aspects of chamber formation. Here, we demonstrate that epigenetic factors also have a significant influence on chamber morphogenesis. Specifically, we show that an atrium-specific contractility defect has a profound impact on ventricular development. We find that the zebrafish locus weak atrium encodes an atrium-specific Myosin heavy chain that is required for Atrial myofibrillar organization and contraction. Despite their Atrial defects, weak atrium mutants can maintain circulation through ventricular contraction. However, the weak atrium mutant ventricle becomes unusually compact, exhibiting a thickened myocardial wall, a narrow lumen and changes in myocardial gene expression. As weak atrium/Atrial Myosin heavy chain is expressed only in the atrium, the ventricular phenotypes in weak atrium mutants represent a secondary response to Atrial dysfunction. Thus, not only is cardiac form essential for cardiac function, but there also exists a reciprocal relationship in which function can influence form. These findings are relevant to our understanding of congenital defects in cardiac chamber morphogenesis.

  • Mutation of weak atrium/Atrial Myosin heavy chain disrupts Atrial function and influences ventricular morphogenesis in zebrafish.
    Development (Cambridge England), 2003
    Co-Authors: Eli Berdougo, Hope Coleman, Diana H Lee, Didier Y R Stainier, Deborah Yelon
    Abstract:

    The embryonic vertebrate heart is composed of two major chambers, a ventricle and an atrium, each of which has a characteristic size, shape and functional capacity that contributes to efficient circulation. Chamber-specific gene expression programs are likely to regulate key aspects of chamber formation. Here, we demonstrate that epigenetic factors also have a significant influence on chamber morphogenesis. Specifically, we show that an atrium-specific contractility defect has a profound impact on ventricular development. We find that the zebrafish locus weak atrium encodes an atrium-specific Myosin heavy chain that is required for Atrial myofibrillar organization and contraction. Despite their Atrial defects, weak atrium mutants can maintain circulation through ventricular contraction. However, the weak atrium mutant ventricle becomes unusually compact, exhibiting a thickened myocardial wall, a narrow lumen and changes in myocardial gene expression. As weak atrium/Atrial Myosin heavy chain is expressed only in the atrium, the ventricular phenotypes in weak atrium mutants represent a secondary response to Atrial dysfunction. Thus, not only is cardiac form essential for cardiac function, but there also exists a reciprocal relationship in which function can influence form. These findings are relevant to our understanding of congenital defects in cardiac chamber morphogenesis.

Dimitris Beis - One of the best experts on this subject based on the ideXlab platform.

  • Ventricular remodeling of single-chambered myh6-/- adult zebrafish hearts occurs via a hyperplastic response and is accompanied by elastin deposition in the atrium.
    Cell and tissue research, 2019
    Co-Authors: Panagiotis Sarantis, Catherine Gaitanaki, Dimitris Beis
    Abstract:

    Zebrafish (Danio rerio) is widely used as an animal model to understand the pathophysiology of cardiovascular diseases. Here, we present the adult cardiac phenotype of weak atrium, myh6-/-, which carry mutations in the zebrafish Atrial Myosin heavy chain. Homozygous mutants survive to adulthood and are fertile despite their initial weak Atrial beat. In adult mutants, the atrium remains hypoplastic and shows elastin deposition while mutant ventricles exhibit increased size. In mammals, hypertrophy is the most common mechanism resulting in cardiomegaly. Using immunohistochemistry and confocal microscopy to measure cardiomyocyte cell size, density and proliferation, we show that the enlargement of the myh6-/- ventricle is predominantly due to hyperplasia. However, we identified similar transcriptional profiles to the mammalian hypertrophy response via RT-PCR of the hyperplastic ventricles. Furthermore, we show activation of the ER-stress pathway by western blot analysis. In conclusion, we can assume, based on our model, that molecular signaling pathways associated with hypertrophy in mammals, in combination with ER-stress activation, result in hyperplasia in zebrafish. In addition, to our knowledge, this is the first time to report elastin deposition in the atrium.

  • ventricular remodeling of single chambered myh6 adult zebrafish hearts occurs via a hyperplastic response and is accompanied by elastin deposition in the atrium
    Cell and Tissue Research, 2019
    Co-Authors: Panagiotis Sarantis, Catherine Gaitanaki, Dimitris Beis
    Abstract:

    Zebrafish (Danio rerio) is widely used as an animal model to understand the pathophysiology of cardiovascular diseases. Here, we present the adult cardiac phenotype of weak atrium, myh6-/-, which carry mutations in the zebrafish Atrial Myosin heavy chain. Homozygous mutants survive to adulthood and are fertile despite their initial weak Atrial beat. In adult mutants, the atrium remains hypoplastic and shows elastin deposition while mutant ventricles exhibit increased size. In mammals, hypertrophy is the most common mechanism resulting in cardiomegaly. Using immunohistochemistry and confocal microscopy to measure cardiomyocyte cell size, density and proliferation, we show that the enlargement of the myh6-/- ventricle is predominantly due to hyperplasia. However, we identified similar transcriptional profiles to the mammalian hypertrophy response via RT-PCR of the hyperplastic ventricles. Furthermore, we show activation of the ER-stress pathway by western blot analysis. In conclusion, we can assume, based on our model, that molecular signaling pathways associated with hypertrophy in mammals, in combination with ER-stress activation, result in hyperplasia in zebrafish. In addition, to our knowledge, this is the first time to report elastin deposition in the atrium.

Panagiotis Sarantis - One of the best experts on this subject based on the ideXlab platform.

  • Ventricular remodeling of single-chambered myh6-/- adult zebrafish hearts occurs via a hyperplastic response and is accompanied by elastin deposition in the atrium.
    Cell and tissue research, 2019
    Co-Authors: Panagiotis Sarantis, Catherine Gaitanaki, Dimitris Beis
    Abstract:

    Zebrafish (Danio rerio) is widely used as an animal model to understand the pathophysiology of cardiovascular diseases. Here, we present the adult cardiac phenotype of weak atrium, myh6-/-, which carry mutations in the zebrafish Atrial Myosin heavy chain. Homozygous mutants survive to adulthood and are fertile despite their initial weak Atrial beat. In adult mutants, the atrium remains hypoplastic and shows elastin deposition while mutant ventricles exhibit increased size. In mammals, hypertrophy is the most common mechanism resulting in cardiomegaly. Using immunohistochemistry and confocal microscopy to measure cardiomyocyte cell size, density and proliferation, we show that the enlargement of the myh6-/- ventricle is predominantly due to hyperplasia. However, we identified similar transcriptional profiles to the mammalian hypertrophy response via RT-PCR of the hyperplastic ventricles. Furthermore, we show activation of the ER-stress pathway by western blot analysis. In conclusion, we can assume, based on our model, that molecular signaling pathways associated with hypertrophy in mammals, in combination with ER-stress activation, result in hyperplasia in zebrafish. In addition, to our knowledge, this is the first time to report elastin deposition in the atrium.

  • ventricular remodeling of single chambered myh6 adult zebrafish hearts occurs via a hyperplastic response and is accompanied by elastin deposition in the atrium
    Cell and Tissue Research, 2019
    Co-Authors: Panagiotis Sarantis, Catherine Gaitanaki, Dimitris Beis
    Abstract:

    Zebrafish (Danio rerio) is widely used as an animal model to understand the pathophysiology of cardiovascular diseases. Here, we present the adult cardiac phenotype of weak atrium, myh6-/-, which carry mutations in the zebrafish Atrial Myosin heavy chain. Homozygous mutants survive to adulthood and are fertile despite their initial weak Atrial beat. In adult mutants, the atrium remains hypoplastic and shows elastin deposition while mutant ventricles exhibit increased size. In mammals, hypertrophy is the most common mechanism resulting in cardiomegaly. Using immunohistochemistry and confocal microscopy to measure cardiomyocyte cell size, density and proliferation, we show that the enlargement of the myh6-/- ventricle is predominantly due to hyperplasia. However, we identified similar transcriptional profiles to the mammalian hypertrophy response via RT-PCR of the hyperplastic ventricles. Furthermore, we show activation of the ER-stress pathway by western blot analysis. In conclusion, we can assume, based on our model, that molecular signaling pathways associated with hypertrophy in mammals, in combination with ER-stress activation, result in hyperplasia in zebrafish. In addition, to our knowledge, this is the first time to report elastin deposition in the atrium.

Eli Berdougo - One of the best experts on this subject based on the ideXlab platform.

  • mutation of weak atrium Atrial Myosin heavy chain disrupts Atrial function and influences ventricular morphogenesis in zebrafish
    Development, 2003
    Co-Authors: Eli Berdougo, Hope Coleman, Diana H Lee, Didier Y R Stainier, Deborah Yelon
    Abstract:

    The embryonic vertebrate heart is composed of two major chambers, a ventricle and an atrium, each of which has a characteristic size, shape and functional capacity that contributes to efficient circulation. Chamber-specific gene expression programs are likely to regulate key aspects of chamber formation. Here, we demonstrate that epigenetic factors also have a significant influence on chamber morphogenesis. Specifically, we show that an atrium-specific contractility defect has a profound impact on ventricular development. We find that the zebrafish locus weak atrium encodes an atrium-specific Myosin heavy chain that is required for Atrial myofibrillar organization and contraction. Despite their Atrial defects, weak atrium mutants can maintain circulation through ventricular contraction. However, the weak atrium mutant ventricle becomes unusually compact, exhibiting a thickened myocardial wall, a narrow lumen and changes in myocardial gene expression. As weak atrium/Atrial Myosin heavy chain is expressed only in the atrium, the ventricular phenotypes in weak atrium mutants represent a secondary response to Atrial dysfunction. Thus, not only is cardiac form essential for cardiac function, but there also exists a reciprocal relationship in which function can influence form. These findings are relevant to our understanding of congenital defects in cardiac chamber morphogenesis.

  • Mutation of weak atrium/Atrial Myosin heavy chain disrupts Atrial function and influences ventricular morphogenesis in zebrafish.
    Development (Cambridge England), 2003
    Co-Authors: Eli Berdougo, Hope Coleman, Diana H Lee, Didier Y R Stainier, Deborah Yelon
    Abstract:

    The embryonic vertebrate heart is composed of two major chambers, a ventricle and an atrium, each of which has a characteristic size, shape and functional capacity that contributes to efficient circulation. Chamber-specific gene expression programs are likely to regulate key aspects of chamber formation. Here, we demonstrate that epigenetic factors also have a significant influence on chamber morphogenesis. Specifically, we show that an atrium-specific contractility defect has a profound impact on ventricular development. We find that the zebrafish locus weak atrium encodes an atrium-specific Myosin heavy chain that is required for Atrial myofibrillar organization and contraction. Despite their Atrial defects, weak atrium mutants can maintain circulation through ventricular contraction. However, the weak atrium mutant ventricle becomes unusually compact, exhibiting a thickened myocardial wall, a narrow lumen and changes in myocardial gene expression. As weak atrium/Atrial Myosin heavy chain is expressed only in the atrium, the ventricular phenotypes in weak atrium mutants represent a secondary response to Atrial dysfunction. Thus, not only is cardiac form essential for cardiac function, but there also exists a reciprocal relationship in which function can influence form. These findings are relevant to our understanding of congenital defects in cardiac chamber morphogenesis.

Didier Y R Stainier - One of the best experts on this subject based on the ideXlab platform.

  • Abstract 283: Nppa Marks A Subset Of Embryonic Cardiomyocytes Predestined To Form Trabeculae In Zebrafish
    Circulation Research, 2014
    Co-Authors: Rima Arnaout, Didier Y R Stainier, Shaun R. Coughlin
    Abstract:

    The development and maintenance of cardiac trabeculae is required for proper ventricular function. Aberrant trabeculation can cause heart failure, arrhythmia, and death. Yet the mechanisms controlling initiation of trabeculation are incompletely understood, partly due to a lack of markers for trabeculation during early embryogenesis. We hypothesized that natriuretic peptide A (nppa) marks trabeculae before cardiomyocytes leave the single-celled ventricular layer. While nppa has been studied in mammals, the external development of the translucent zebrafish embryo offers new insight into the earliest stages of trabeculation. We have found by in situ hybridization, and by creating a fluorescent transgenic zebrafish line, that nppa exclusively marks zebrafish cardiac trabeculae from their onset through adulthood. Live spinning disc confocal video microscopy shows that nppa:GFP-positive cells move into the trabecular layer starting at 60 hours post fertilization (hpf). GFP-positive trabeculae are seen by 5 days post fertilization (dpf) in normal larvae. However, in cardiac troponin T2a mutants and in erbB2 mutants _ both known not to trabeculate _ nppa is still expressed, but the nppa:GFP positive cells fail to form trabecular projections. In embryos injected with a morpholino against Atrial Myosin heavy chain 6, where weakened Atrial contraction leads to weaker blood flow without affecting the ventricle directly, GFP-positive cells form trabeculae similar to uninjected controls. Using Clustered Regularly Interspaced Short Palindromic Repeats (CRISPRs), we created nppa mutants causing frameshift deletions. Mutants have poorly contractile hearts at 3 dpf and have been crossed into transgenic reporter lines in order to specifically assess trabeculation. Together, these data suggest that nppa marks a subset of embryonic cardiomyocytes destined to form trabeculae, and that nppa loss of function causes cardiac defects.

  • mutation of weak atrium Atrial Myosin heavy chain disrupts Atrial function and influences ventricular morphogenesis in zebrafish
    Development, 2003
    Co-Authors: Eli Berdougo, Hope Coleman, Diana H Lee, Didier Y R Stainier, Deborah Yelon
    Abstract:

    The embryonic vertebrate heart is composed of two major chambers, a ventricle and an atrium, each of which has a characteristic size, shape and functional capacity that contributes to efficient circulation. Chamber-specific gene expression programs are likely to regulate key aspects of chamber formation. Here, we demonstrate that epigenetic factors also have a significant influence on chamber morphogenesis. Specifically, we show that an atrium-specific contractility defect has a profound impact on ventricular development. We find that the zebrafish locus weak atrium encodes an atrium-specific Myosin heavy chain that is required for Atrial myofibrillar organization and contraction. Despite their Atrial defects, weak atrium mutants can maintain circulation through ventricular contraction. However, the weak atrium mutant ventricle becomes unusually compact, exhibiting a thickened myocardial wall, a narrow lumen and changes in myocardial gene expression. As weak atrium/Atrial Myosin heavy chain is expressed only in the atrium, the ventricular phenotypes in weak atrium mutants represent a secondary response to Atrial dysfunction. Thus, not only is cardiac form essential for cardiac function, but there also exists a reciprocal relationship in which function can influence form. These findings are relevant to our understanding of congenital defects in cardiac chamber morphogenesis.

  • Mutation of weak atrium/Atrial Myosin heavy chain disrupts Atrial function and influences ventricular morphogenesis in zebrafish.
    Development (Cambridge England), 2003
    Co-Authors: Eli Berdougo, Hope Coleman, Diana H Lee, Didier Y R Stainier, Deborah Yelon
    Abstract:

    The embryonic vertebrate heart is composed of two major chambers, a ventricle and an atrium, each of which has a characteristic size, shape and functional capacity that contributes to efficient circulation. Chamber-specific gene expression programs are likely to regulate key aspects of chamber formation. Here, we demonstrate that epigenetic factors also have a significant influence on chamber morphogenesis. Specifically, we show that an atrium-specific contractility defect has a profound impact on ventricular development. We find that the zebrafish locus weak atrium encodes an atrium-specific Myosin heavy chain that is required for Atrial myofibrillar organization and contraction. Despite their Atrial defects, weak atrium mutants can maintain circulation through ventricular contraction. However, the weak atrium mutant ventricle becomes unusually compact, exhibiting a thickened myocardial wall, a narrow lumen and changes in myocardial gene expression. As weak atrium/Atrial Myosin heavy chain is expressed only in the atrium, the ventricular phenotypes in weak atrium mutants represent a secondary response to Atrial dysfunction. Thus, not only is cardiac form essential for cardiac function, but there also exists a reciprocal relationship in which function can influence form. These findings are relevant to our understanding of congenital defects in cardiac chamber morphogenesis.