Vascular endothelial growth factor receptor signaling is required for cardiac valve formation in zebrafish

Lee, You Mie; Cope, John J.; Ackermann, Gabriele E.; Goishi, Katsutoshi; Armstrong, Ehrin J.; Paw, Barry H.; Bischoff, Joyce

doi:10.1002/dvdy.20559

Cited by 44 publications

(37 citation statements)

References 33 publications

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“…For example, myocardialendocardial communication mediated by Tgf-␤, Wnt, Notch, Calcineurin and Vegf signaling is crucial during atrioventricular valve formation (e.g. Armstrong and Bischoff, 2004;Beis et al, 2005;Chang et al, 2004;Hurlstone et al, 2003;Lee et al, 2006;Timmerman et al, 2004). Additionally, Neuregulin and PlexinSemaphorin signaling are crucial during trabecular outgrowth (Meyer et al, 1997;Toyofuku et al, 2004), Neuregulin and Notch signaling are crucial during specification of the cardiac conduction system (Milan et al, 2006;Rentschler et al, 2002), and Heart of glass signaling is crucial during chamber wall thickening (Mably et al, 2003).…”

Section: Research Articlementioning

confidence: 99%

Endocardium is necessary for cardiomyocyte movement during heart tube assembly

et al. 2007

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Embryonic heart formation requires the union of bilateral populations of cardiomyocytes and their reorganization into a simple tube. Little is known about the morphogenetic mechanisms that coordinate assembly of the heart tube and determine its dimensions. Using time-lapse confocal microscopy to track individual cardiomyocyte movements in the zebrafish embryo, we identify two morphologically and genetically separable phases of cell movement that coordinate heart tube assembly. First, all cardiomyocytes undergo coherent medial movement. Next, peripherally located cardiomyocytes change their direction of movement, angling toward the endocardial precursors and thereby establishing the initial circumference of the nascent heart tube. These two phases of cardiomyocyte behavior are independently regulated. Furthermore, we find that myocardial-endocardial interactions influence the second phase by regulating the induction, direction and duration of cardiomyocyte movement. Thus, the endocardium plays a crucial early role in cardiac morphogenesis, organizing cardiomyocytes into a configuration appropriate for heart tube assembly. Together, our data reveal a dynamic cellular mechanism by which tissue interactions establish organ architecture.

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Section: Research Articlementioning

confidence: 99%

Endocardium is necessary for cardiomyocyte movement during heart tube assembly

et al. 2007

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“…Within this process, the cushions must be populated by cells predominantly recruited from the cushion endocardium through epithelial-mesenchymal transformation (EMT). A role for VEGF in atrioventricular cushion EMT has been shown, albeit both stimulating 10,11 and inhibiting. 12 This led to the hypothesis that VEGF must be expressed within a "physiological window" during cushion development.…”

mentioning

confidence: 99%

Tetralogy of Fallot and Alterations in Vascular Endothelial Growth Factor-A Signaling and Notch Signaling in Mouse Embryos Solely Expressing the VEGF120 Isoform

Akker

Molin

Peters

et al. 2007

Circulation Research

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Abstract-The importance of vascular endothelial growth factor-A (VEGF) and subsequent Notch signaling in cardiac outflow tract development is generally recognized. Although genetic heterogeneity and mutations of these genes in both humans and mouse models relate to a high susceptibility to develop outflow tract malformations such as tetralogy of Fallot and peripheral pulmonary stenosis, no etiology has been proposed so far.

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“…Previous studies have shown that myocardial Nfat2/3/4 represses Vegf expression in the AVC that allows local EMT, and that later endocardial Calcineurin-Nfatc1 promotes valve elongation and remodeling in mice (Chang et al, 2004). Early studies suggested that VEGF-Nfatc1 is essential for endocardial cell proliferation (Lee et al, 2006;Combs and Yutzey, 2009b). On the other hand, others reported that VEGF is dispensable for endocardial cell proliferation, cell death and Nfatc1 nuclear localization in the endocardial cells of elongating mitral valves (Stankunas et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Scl/tal1 is not needed for the formation of endocardial progenitors but is essential for endocardial cell migration (Bussmann et al, 2007). While VEGF-induced NFATc1 activation promotes endocardial cell proliferation for sustaining endocardial cell numbers in heart valve development (Combs and Yutzey, 2009b;Graef et al, 2001;Johnson et al, 2003;Lee et al, 2006), we have limited knowledge on how endocardial cell proliferation is regulated before and during the formation of the atrio-ventricular canal (AVC) and cardiac valves. The common cardinal vein (CCV) is on the yolk syncytial layer connecting the posterior cardinal vein (PCV) and the sinus venosus of the heart.…”

Section: Introductionmentioning

confidence: 99%

Genetic Interaction between pku300 and fbn2b Controls Endocardial Cell Proliferation and Valve Development in Zebrafish

Wang

et al. 2013

Journal of Cell Science

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SummaryAbnormal cardiac valve morphogenesis is a common cause of human congenital heart disease. The molecular mechanisms regulating endocardial cell proliferation and differentiation into cardiac valves remain largely unknown, although great progress has been made on the endocardial contribution to the atrioventricular cushion and valve formation. We found that scotch tape te382 (sco te382 ) encodes a novel transmembrane protein that is crucial for endocardial cell proliferation and heart valve development. The zebrafish sco te382 mutant showed diminished endocardial cell proliferation, lack of heart valve leaflets and abnormal common cardinal and caudal veins. Positional cloning revealed a C946T nonsense mutation of a novel gene pku300 in the sco te382 locus, which encoded a 540-amino-acid protein on cell membranes with one putative transmembrane domain and three IgG domains. A known G3935T missense mutation of fbn2b was also found ,570 kb away from pku300 in sco te382 mutants. The genetic mutant sco pku300 , derived from sco te382 , only had the C946T mutation of pku300 and showed reduced numbers of atrial endocardial cells and an abnormal common cardinal vein. Morpholino knockdown of fbn2b led to fewer atrial endocardial cells and an abnormal caudal vein. Knockdown of both pku300 and fbn2b phenocopied these phenotypes in sco te382 genetic mutants. pku300 transgenic expression in endocardial and endothelial cells, but not myocardial cells, partially rescued the atrial endocardial defects in sco te382 mutants. Mechanistically, pku300 and fbn2b were required for endocardial cell proliferation, endocardial Notch signaling and the proper formation of endocardial cell adhesion and tight junctions, all of which are crucial for cardiac valve development. We conclude that pku300 and fbn2b represent the few genes capable of regulating endocardial cell proliferation and signaling in zebrafish cardiac valve development.

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Vascular endothelial growth factor receptor signaling is required for cardiac valve formation in zebrafish

Cited by 44 publications

References 33 publications

Endocardium is necessary for cardiomyocyte movement during heart tube assembly

Endocardium is necessary for cardiomyocyte movement during heart tube assembly

Tetralogy of Fallot and Alterations in Vascular Endothelial Growth Factor-A Signaling and Notch Signaling in Mouse Embryos Solely Expressing the VEGF120 Isoform

Genetic Interaction between pku300 and fbn2b Controls Endocardial Cell Proliferation and Valve Development in Zebrafish

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