Trabeculated Right Ventricular Free Wall in the Chicken Heart Forms by Ventricularization of the Myocardium Initially Forming the Outflow Tract

Rana, M. Sameer; Horsten, Noortje C.A.; Tesink-Taekema, Sabina; Lamers, W. H.; Moorman, Antoon F.M.; Hoff, Maurice J.B. van den

doi:10.1161/01.res.0000262688.14288.b8

Cited by 66 publications

(64 citation statements)

References 46 publications

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“…There is support from our studies that lengthening of the subpulmonary myocardium of the OFT is active until day 12.5, which is at least one day longer than posed in the literature (Xu et al, 2004;Viragh and Challice 1973) but in line with studies in chick that have indicated contributions to the OFT up to HH24 (correlating with mouse day12.5) (Rana et al, 2007).…”

Section: Developmental Dynamicssupporting

confidence: 90%

“…Although the exact time span of cellular addition from the anterior heart field to the myocardial OFT is unclear, addition until embryonic day (E) 11.5 in mouse was previously described (Xu et al, 2004). Using immunofluorescent stainings and deposits of Indian ink in chick, an increase of the myocardial part of the OFT up to stage HH24 has been demonstrated (Rana et al, 2007), corresponding to E12.5 in mouse.…”

Section: Introductionmentioning

confidence: 98%

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Morphogenesis of outflow tract rotation during cardiac development: The pulmonary push concept

Scherptong

Jongbloed

Wisse

et al. 2012

Developmental Dynamics

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Background: Understanding of cardiac outflow tract (OFT) remodeling is essential to explain repositioning of the aorta and pulmonary orifice. In wild type embryos (E9.5-14.5), second heart field contribution (SHF) to the OFT was studied using expression patterns of Islet 1, Nkx2.5, MLC-2a, WT-1, and 3D-reconstructions. Abnormal remodeling was studied in VEGF120/120 embryos. Results: In wild type, Islet 1 and Nkx2.5 positive myocardial precursors formed an asymmetric elongated column almost exclusively at the pulmonary side of the OFT up to the pulmonary orifice. In VEGF120/120 embryos, the Nkx2.5-positive mesenchymal population was disorganized with a short extension along the pulmonary OFT. Conclusions: We postulate that normally the pulmonary trunk and orifice are pushed in a higher and more frontal position relative to the aortic orifice by asymmetric addition of SHF-myocardium. Deficient or disorganized right ventricular OFT expansion might explain cardiac malformations with abnormal position of the great arteries, such as double outlet right ventricle. Developmental Dynamics 241:1413-1422, 2012. V C 2012 Wiley Periodicals, Inc.Key words: cardiac development; outflow tract; gene expression Key findings:The addition of Nkx2.5-positive myocardial precursors from the anterior heart field occurs during normal development in an asymmetrical fashion, predominantly below the left branch of the 6th pharyngeal arch artery. The continued addition of right-sided myocardium during normal development results in movement without spiralization of the OFT in which the pulmonary trunk orifice is pushed in a rightward and anterior direction, a mechanism referred to as ''pulmonary push.'' Deficient or disorganized positioning of the Nkx2.5-positive precursors, as was observed in VEGF120/120 mutants might explain cardiac malformations with side-by-side position of the great arteries, such as double outlet right ventricle.

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Section: Developmental Dynamicssupporting

confidence: 90%

Section: Introductionmentioning

confidence: 98%

Morphogenesis of outflow tract rotation during cardiac development: The pulmonary push concept

Scherptong

Jongbloed

Wisse

et al. 2012

Developmental Dynamics

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“…However, we observed an unexpectedly large part of the left ventricular wall to be derived from the embryonic Tbx2 ϩ AVC, whereas the embryonic ventricle, generally assumed to be the precursor compartment of the definitive left ventricle, 20,21,27 only gave rise to the apex, left ventricular septum, and AV bundle. We confirmed the physical relation between the E9.5 AVC and E10.5 left ventricular wall (base) by DiI labeling.…”

Section: Origin and Fate Of The Tbx2mentioning

confidence: 71%

“…Consistently, the primary outflow tract was found to "disappear" mainly through continuous differentiation to ventricular myocardium, with integration of cells into the right ventricular chamber. 27 We propose that slowly proliferating Tbx2 ϩ primary myocardial AVC, inner curvature, and outflow tract cells are marked by Tbx2-Cre. Subsequently, primary myocardial cells (or their daughters) at the border with the ventricular chambers differentiate to Tbx2-negative fast-proliferating chamber myocardium, integrate into the chambers, and rapidly expand to provide a large contribution to the ventricles ( Figure 6A).…”

Section: A Model For Chamber Formation From Primary Myocardiummentioning

confidence: 91%

The Tbx2 ⁺ Primary Myocardium of the Atrioventricular Canal Forms the Atrioventricular Node and the Base of the Left Ventricle

Aanhaanen

Brons

Domínguez³

et al. 2009

Circulation Research

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157

182

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Abstract-The primary myocardium of the embryonic heart, including the atrioventricular canal and outflow tract, is essential for septation and valve formation. In the chamber-forming heart, the expression of the T-box transcription factor Tbx2 is restricted to the primary myocardium. To gain insight into the cellular contributions of the Tbx2 ϩ primary myocardium to the components of the definitive heart, genetic lineage tracing was performed using a novel Tbx2 Cre allele. These analyses revealed that progeny of Tbx2 ϩ cells provide an unexpectedly large contribution to the Tbx2-negative ventricles. Contrary to common assumption, we found that the embryonic left ventricle only forms the left part of the definitive ventricular septum and the apex. The atrioventricular node, but not the atrioventricular bundle, was found to derive from Tbx2 ϩ cells. The Tbx2 ϩ outflow tract formed the right ventricle and right part of the ventricular septum. In Tbx2-deficient embryos, the left-sided atrioventricular canal was found to prematurely differentiate to chamber myocardium and to proliferate at increased rates similar to those of chamber myocardium. As a result, the atrioventricular junction and base of the left ventricle were malformed. Together, these observations indicate that Tbx2 temporally suppresses differentiation and proliferation of primary myocardial cells. A subset of these Tbx2Cre -marked cells switch off expression of Tbx2, which allows them to differentiate into chamber myocardium, to initiate proliferation, and to provide a large contribution to the ventricles. These findings imply that errors in the development of the early atrioventricular canal may affect a much larger region than previously anticipated, including the ventricular base. Key Words: atrioventricular canal Ⅲ lineage Ⅲ fate Ⅲ patterning Ⅲ transgenic Ⅲ Cre T he embryonic heart tube is composed of "primary" myocardium and rapidly elongates by addition of progenitor cells to its poles. During looping, specific regions in the embryonic tubular heart differentiate to chamber myocardium and expand to form the future working myocardium of the ventricles and atria. In contrast, the region in between these expanding chambers does not differentiate or expand and becomes visible as an atrioventricular constriction. 1 During prenatal life, the atrioventricular canal (AVC) myocardium conducts the electric impulse between the atrial and ventricular chambers in a slow manner, reminiscent of the function of the mature atrioventricular (AV) node. This slow conducting feature allows the AVC to act as a sphincter preventing backflow from the ventricles to the atria, analogous to the AV valves. Furthermore, the primary myocardium provides the signals that initiate formation of the cushions, which subsequently will form the valves and partake in septation. 2,3 The primary myocardial AVC is extensively remodeled to properly connect and align both atria and ventricles and to coordinate the formation of the fibrous insulation. 4 Given all these roles of the AV...

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“…Also, in chicken, it has been shown that cells of the SHF populate the right ventricle. 14 In frogs, that have just one ventricle, cells of the SHF exclusively end up in the OFT. 15 The LIM homeodomain transcription factor Islet (Isl)1 has become a popular molecular marker demarcating the SHF.…”

Section: Early Heart Development: From a Common Progenitor To Differementioning

confidence: 99%

The Multiple Phases and Faces of Wnt Signaling During Cardiac Differentiation and Development

Gessert

Kühl

2010

Circulation Research

359

310

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Understanding heart development on a molecular level is a prerequisite for uncovering the causes of congenital heart diseases. Therapeutic approaches that try to enhance cardiac regeneration or that involve the differentiation of resident cardiac progenitor cells or patient-specific induced pluripotent stem cells will also benefit tremendously from this knowledge. Wnt proteins have been shown to play multiple roles during cardiac differentiation and development. They are extracellular growth factors that activate different intracellular signaling branches. Here, we summarize our current understanding of how these factors affect different aspects of cardiogenesis, starting from early specification of cardiac progenitors and continuing on to later developmental steps, such as morphogenetic processes, valve formation, and establishment of the conduction system. (Circ Res. 2010;107:186-199.)

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Trabeculated Right Ventricular Free Wall in the Chicken Heart Forms by Ventricularization of the Myocardium Initially Forming the Outflow Tract

Cited by 66 publications

References 46 publications

Morphogenesis of outflow tract rotation during cardiac development: The pulmonary push concept

Morphogenesis of outflow tract rotation during cardiac development: The pulmonary push concept

The Tbx2 ⁺ Primary Myocardium of the Atrioventricular Canal Forms the Atrioventricular Node and the Base of the Left Ventricle

The Multiple Phases and Faces of Wnt Signaling During Cardiac Differentiation and Development

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Trabeculated Right Ventricular Free Wall in the Chicken Heart Forms by Ventricularization of the Myocardium Initially Forming the Outflow Tract

Cited by 66 publications

References 46 publications

Morphogenesis of outflow tract rotation during cardiac development: The pulmonary push concept

Morphogenesis of outflow tract rotation during cardiac development: The pulmonary push concept

The Tbx2 + Primary Myocardium of the Atrioventricular Canal Forms the Atrioventricular Node and the Base of the Left Ventricle

The Multiple Phases and Faces of Wnt Signaling During Cardiac Differentiation and Development

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The Tbx2 ⁺ Primary Myocardium of the Atrioventricular Canal Forms the Atrioventricular Node and the Base of the Left Ventricle