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At least 343 records · Page 19Linked to original sources
PubMed1991

Detection of myosin gene expression in the developing heart using probes derived by polymerase chain reaction.

The polymerase chain reaction provides a rapid method for the molecular cloning of DNA probes suitable for the detection of specific messenger RNA. We have used this approach to prepare probes specific for human cardiac myosin messenger RNA and demonstrate here the use of such probes in the analysis of human cardiac development by hybridization in situ to sections of fetal tissue. This combination of techniques is suitable for the detection of any messenger RNA for which sequence data are available, and offers a powerful new approach to the analysis of cardiac development.

Fetal Heart↗
PubMed2000

BMP2 is required for early heart development during a distinct time period.

BMP2, like its Drosophila homologue dpp, is an important signaling molecule for specification of cardiogenic mesoderm in vertebrates. Here, we analyzed the time-course of BMP2-requirement for early heart formation in whole chick embryos and in explants of antero-lateral plate mesoderm. Addition of Noggin to explants isolated at stage 4 and cultured for 24 h resulted in loss of NKX2.5, GATA4, eHAND, Mef2A and vMHC expression. At stages 5-8 the individual genes showed differential sensitivity to Noggin addition. While expression of eHAND, NKX2.5 and Mef2A was clearly reduced by Noggin vMHC was only marginally affected. In contrast, GATA4 expression was enhanced after Noggin treatment. The developmental period during which cardiac mesoderm required the presence of BMP signaling in vivo was assessed by implantation of Noggin expressing cells into stage 4-8 embryos which were then cultured until stage 10-11. Complete loss of NKX2.5 and eHAND expression was observed in embryos implanted at stages 4-6, and expression was still suppressed in stages 7 and 8 implanted embryos. GATA4 expression was also blocked by Noggin at stage 4, however increased at stages 5, 6 and 7. Explants of central mesendoderm, that normally do not form heart tissue were employed to study the time-course of BMP2-induced cardiac gene expression. The induction of cardiac lineage markers in central mesendoderm of stage 5 embryos was distinct for different genes. While GATA4, -5, -6 and MEF2A were induced to maximal levels within 6 h after BMP2 addition, eHAND and dHAND required 12 h to reach maximum levels of expression. NKX2.5 was induced by 6 h and accumulated over 48 h. vMHC and titin were induced at significant levels only after 48 h of BMP2 addition. These results indicate that cardiac marker genes display distinct expression kinetics after BMP2 addition and differential response to Noggin treatment suggesting complex regulation of myocardial gene expression in the early tubular heart.

Animals↗
PubMed1991

Heart development in normal and cardiac-lethal mutant axolotls: a model for the control of vertebrate cardiogenesis.

The mechanisms which regulate myocardial differentiation are poorly understood. The cardiac-lethal (c) mutant of Ambystoma mexicanum, in which the heart never begins to beat, provides a valuable model system for studying this process. Using an in vitro assay, we examine the nature of the defect in c/c embryos and find (contrary to previous reports) that the inductive endoderm is not affected by the mutation. Rather, the pre-cardiac mesoderm is directly affected by the c gene and is incapable of responding to normal inductive influences. Furthermore, we find that mutant mesoderm can complete its differentiation into functional cardiomyocytes when co-cultured with wild-type heart mesoderm. With this evidence, we propose a model for the regulation of heart differentiation based on the migration of the heart mesoderm over a gradient of inducer, and the subsequent establishment of a two-component reaction-diffusion system within the mesoderm itself. This model has the potential to explain several poorly understood aspects of cardiogenesis, including the gradual nature of heart induction, the restriction of the heart field, and possibly the early morphogenesis of the heart tube.

Ambystoma mexicanum↗
PubMed2005

Selective role of a distinct tyrosine residue on Tie2 in heart development and early hematopoiesis.

The development of the cardiovascular system and the development of the early hematopoietic systems are closely related, and both require signaling through the Tie2 receptor tyrosine kinase. Although endothelial cells and hematopoietic cells as well as their precursors share common gene expression patterns during development, it remains completely unknown how Tie2 signaling coordinately regulates cardiovascular development and early hematopoiesis in vivo. We show here that mice with a targeted mutation in tyrosine residue 1100 in the carboxyl-terminal tail of Tie2 display defective cardiac development and impaired hematopoietic and endothelial cell development in the paraaortic splanchnopleural mesoderm similar to that seen in Tie2-null mutant mice. Surprisingly, however, unlike Tie2-null mutant mice, mice deficient in signaling through this tyrosine residue show a normal association of perivascular cells with nascent blood vessels. These studies are the first to demonstrate the physiological importance of a single tyrosine residue in Tie2, and they suggest that multiple tyrosine residues in the receptor may coordinate cardiovascular development and early hematopoietic development.

Animals↗
PubMed2003

Fetal heart development in the nitrofen-induced CDH rat model: the role of mechanical and nonmechanical factors.

BACKGROUND/PURPOSE: In congenital diaphragmatic hernia (CDH), it was recently shown that early and late gestational lung underdevelopment is caused by nonmechanical and mechanical factors, respectively. Heart underdevelopment, which might predict lung hypoplasia, is commonly attributed to mechanical factors. The authors analyzed whether nonmechanical and mechanical factors affect cardiac growth and correlations between lung and heart weights during gestation. METHODS: Left-sided CDH was induced in pregnant Wistar rats by administration of nitrofen on E9.5. At selected gestational ages (E18, E20, and E22), the lungs and heart were harvested, weighed, and analyzed for DNA and protein contents. Left lung and heart weights were correlated at those gestational ages. Two experimental groups: nitrofen without CDH (nitrofen), and nitrofen with CDH (CDH), were compared with normal controls. RESULTS: At E18, both nitrofen-exposed groups presented similar and significant left lung (LL) hypoplasia. As gestation progressed (E20 and E22), in the nitrofen group left lung (LL) hypoplasia decreased, whereas in the CDH group LL hypoplasia was exacerbated relative to normal controls. In contrast, at E18 and E20, heart-to-body weight ratios as well as cardiac DNA and protein contents were reduced significantly in all animals exposed to nitrofen, with no significant differences observed between nitrofen and CDH groups. As gestation progressed, the difference between cardiac parameters in nitrofen-exposed and normal control rats diminished, and at E22 no significant differences were documented. In the CDH group, significant correlations were seen between lung and heart weights at E18 (r = 0.65; P <.05) and E20 (r = 0.4; P <.05), whereas at term gestation (E22) no significant correlation was observed (r = 0.21, not significant). CONCLUSIONS: Nonmechanical factors, which might be directed by nitrofen, play a role in the pathogenesis of lung and heart hypoplasia manifested precociously in fetal life, whereas mechanical compression might influence only lung growth during late gestation. Heart weight predicts lung weight only in early gestational ages.

Animals↗
PubMed1994

Patterns of form and function in developing hearts: contributions from non-mammalian vertebrates.

Although most research on developmental cardiovascular physiology has focused on the bird embryo as a model for emulating developmental processes in mammals, there are increasingly compelling reasons to expand research to a variety of lower vertebrate systems. These reasons include circumventing inherent limitations of the avian embryo and identifying general vertebrate developmental patterns in the cardiovascular system. In this paper, we first review data from hemodynamic studies on amphibians and birds (and what little exists from fish and reptiles), to provide a background against which lower vertebrate development can be examined. We then describe non-mammalian, non-avian paradigms for studying developmental patterns of vertebrate hearts. Developmental spects of cardiovascular performance, especially heart rate, blood pressure and cardiac output and how they change with ontogeny, are described for several amphibians and a few reptiles, identifying, where possible, processes in common with birds and mammals. Finally, we indicate productive areas for future research with lower vertebrate cardiovascular systems, such as establishing "critical windows" for cardiovascular physiology during development, and determining the extent of developmental plasticity at the level of organ system physiology.

Animals↗