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Four-chambered Heart (four-chambered + heart)

Distribution by Scientific Domains

Life Sciences	75%

Selected Abstracts

Second lineage of heart forming region provides new understanding of conotruncal heart defects

CONGENITAL ANOMALIES, Issue 1 2010
Yuji Nakajima
ABSTRACT Abnormal heart development causes various congenital heart defects. Recent cardiovascular biology studies have elucidated the morphological mechanisms involved in normal and abnormal heart development. The primitive heart tube originates from the lateral-most part of the heart forming mesoderm and mainly gives rise to the left ventricle. Then, during the cardiac looping, the outflow tract is elongated by the addition of cardiogenic cells from the both pharyngeal and splanchnic mesoderm (corresponding to anterior and secondary heart field, respectively), which originate from the mediocaudal region of the heart forming mesoderm and are later located anteriorly (rostrally) to the dorsal region of the heart tube. Therefore, the heart progenitors that contribute to the outflow tract region are distinct from those that form the left ventricle. The knowledge that there are two different lineages of heart progenitors in the four-chambered heart provides new understanding of the morphological and molecular etiology of conotruncal heart defects. [source]

Understanding heart development and congenital heart defects through developmental biology: A segmental approach

CONGENITAL ANOMALIES, Issue 4 2005
Masahide Sakabe
ABSTRACT The heart is the first organ to form and function during development. In the pregastrula chick embryo, cells contributing to the heart are found in the postero-lateral epiblast. During the pregastrula stages, interaction between the posterior epiblast and hypoblast is required for the anterior lateral plate mesoderm (ALM) to form, from which the heart will later develop. This tissue interaction is replaced by an Activin-like signal in culture. During gastrulation, the ALM is committed to the heart lineage by endoderm-secreted BMP and subsequently differentiates into cardiomyocyte. The right and left precardiac mesoderms migrate toward the ventral midline to form the beating primitive heart tube. Then, the heart tube generates a right-side bend, and the d-loop and presumptive heart segments begin to appear segmentally: outflow tract (OT), right ventricle, left ventricle, atrioventricular (AV) canal, atrium and sinus venosus. T-box transcription factors are involved in the formation of the heart segments: Tbx5 identifies the left ventricle and Tbx20 the right ventricle. After the formation of the heart segments, endothelial cells in the OT and AV regions transform into mesenchyme and generate valvuloseptal endocardial cushion tissue. This phenomenon is called endocardial EMT (epithelial-mesenchymal transformation) and is regulated mainly by BMP and TGF,. Finally, heart septa that have developed in the OT, ventricle, AV canal and atrium come into alignment and fuse, resulting in the completion of the four-chambered heart. Altered development seen in the cardiogenetic process is involved in the pathogenesis of congenital heart defects. Therefore, understanding the molecular nature regulating the ,nodal point' during heart development is important in order to understand the etiology of congenital heart defects, as well as normal heart development. [source]

Left-asymmetric expression of Galanin in the linear heart tube of the mouse embryo is independent of the nodal co-receptor gene cryptic

DEVELOPMENTAL DYNAMICS, Issue 12 2008
Axel Schweickert
Abstract Only very few left/right asymmetrically expressed genes are known in the mammalian embryo. In a screen for novel factors we identified the gene encoding the neuropeptide Galanin in mouse. At embryonic day (E) 8.5 asymmetric mRNA transcription was found in the left half of the linear heart tube. During heart looping and morphogenesis expression became restricted to the atrio-ventricular (AV) canal, followed by specific staining of the AV-node and AV-rings in the four-chambered heart. Expression was inverted in inv/inv and randomized in homozygous iv mutant embryos. Left-sided heart-specific transcription of mouse Gal thus should be controlled by the left-right pathway. The asymmetric pattern was retained in cryptic mutant embryos, in which the Nodal signaling cascade is disrupted. Surprisingly, Pitx2c was found to be expressed in 50% of cryptic mutant hearts as well, suggesting that some aspects of asymmetric gene expression in the heart are independent of cryptic. Developmental Dynamics 237:3557,3564, 2008. © 2008 Wiley-Liss, Inc. [source]

Cell death and differentiation in the development of the endocardial cushion of the embryonic heart

MICROSCOPY RESEARCH AND TECHNIQUE, Issue 5 2002
Eltyeb Abdelwahid
Abstract The transformation of the endocardial cushion into valves and septa is a critical step in cardiac morphogenesis as it initiates the development of the four-chambered heart. This transformation results from a region-specific balance between cellular proliferation, apoptosis, and differentiation. The development of the form and structure of the endocardial cushion is accompanied by precise patterns of abundant cell death having the morphological features of programmed cell death (apoptosis), which plays an important role in the elimination of redundant cells and in changes of phenotypic composition during histogenesis. Apoptosis is an essential process in morphogenesis as it balances mitosis in renewing tissues. It is controlled by one or more genetic programs that kill the targeted cell. However, the causes, role, and regulation of apoptosis in the developing endocardial cushion still remain to be determined. The clarification of the role of the apoptosis regulatory genes constitutes a major task in future studies of cell death in the developing heart. This new molecular histology of heart development awaits further experiments to clarify the interactive mechanisms that act to ensure the sculpting of the endocardial cushion into valves and septa by determining the size of the cushion cell populations. The relation between the expression of different factors and the modifications of the cushion region during cardiac development are reviewed. In addition, we review and summarize information on molecules identified in our experiments that imply the activity of a number of essential genes coinciding with the key steps in generating the overall architecture of the heart. We correlate their temporal and spatial expression with their proposed roles. Microsc. Res. Tech. 58:395,403, 2002. © 2002 Wiley-Liss, Inc. [source]