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At least 397 records · Page 22Linked to original sources
PubMed1996

Vertebrate heart development.

This review summarizes recent studies of the cellular and molecular events involved in the determination and differentiation of cardiac myocytes in vertebrate embryos. Fate-mapping studies in mouse, chick, amphibian and zebrafish embryos suggest that cardiac muscle precursors are specified shortly before or at the time of gastrulation. Nuclear factors, such as dHAND, aryl hydrocarbon receptor, GATA-6, Nkx-2.3, growth arrest homeobox (Gax) and cardiac adriamycin responsive protein (CARP), which have recently been described as playing a role in the commitment and/or differentiation of cardiac myocytes are discussed.

Amphibians↗
PubMed1997

Retroviral techniques for studying organogenesis with a focus on heart development.

The study of development has been revolutionized by the application of molecular techniques, which make it possible to identify factors involved in the developmental process. However, in order to correctly assess the contribution of these growth factors, transcription factors, receptors or signaling molecules, it is necessary to study them in the animal as a whole; it is not enough to conclude that they must be important based on their expression patterns.

Animals↗
PubMed1980

[Morphologic analysis of heart development in the chick embryo].

The skeletal muscle is determined under the influence of the earliest pioneer nerve fibers which grow from the neural tube before the 35th incubation hour in the chick embryo. As far as the myocardial determination is concerned, an initial groove influence on the mesodermal cells of the presumptive cardiac area can be postulated. It may also be pointed out that, at the stage of 6-7 somites, neural crest cells come into contact with splanchnopleural cells. Both of these contacts may be regarded as possible myogenic starters of the heat bud and they are not mutually exclusive.

Animals↗
PubMed1996

Overexpression of the Xenopus Xl-fli gene during early embryogenesis leads to anomalies in head and heart development and erythroid differentiation.

The product of the Xl-fli gene, a Xenopus laevis transcription factor of the ets family, specifically expressed in several lineage of migratory cells during Xenopus development (Meyer et al., Int. J. Dev. Biol. 39: 909-919, 1995) was overproduced during Xenopus embryogenesis, upon microinjection of a synthetic transcript in the fertilized egg or in the early embryo. This results in anomalies of the antero-posterior and dorso-ventral polarities, and in tissue differentiation, particularly in the eye- and head cartilage development, as well as erythroid differentiation (absence of erythrocyte differentiation in the circulating blood, often accompanied by ectopic localization of mature erythrocytes, leading to important hemangiomas). Cytological examination reveals at gastrulation the existence of abnormal cells separating the different embryonic layers, suggesting modifications of the cellular adhesion properties. The possible involvement of the fli gene in controlling the dissemination of migratory cells is discussed.

Animals↗
PubMed2000

Endoglin, an ancillary TGFbeta receptor, is required for extraembryonic angiogenesis and plays a key role in heart development.

Endoglin (CD105) is expressed on the surface of endothelial and haematopoietic cells in mammals and binds TGFbeta isoforms 1 and 3 in combination with the signaling complex of TGFbeta receptors types I and II. Endoglin expression increases during angiogenesis, wound healing, and inflammation, all of which are associated with TGFbeta signaling and alterations in vascular structure. The importance of endoglin for normal vascular architecture is further indicated by the association of mutations in the endoglin gene with the inherited disorder Hereditary Haemorrhagic Telangiectasia Type 1 (HHT1), a disease characterised by bleeding from vascular malformations. In order to study the role of endoglin in vivo in more detail and to work toward developing an animal model of HHT1, we have derived mice that carry a targeted nonsense mutation in the endoglin gene. Studies on these mice have revealed that endoglin is essential for early development. Embryos homozygous for the endoglin mutation fail to progress beyond 10.5 days postcoitum and fail to form mature blood vessels in the yolk sac. This phenotype is remarkably similar to that of the TGFbeta1 and the TGFbeta receptor II knockout mice, indicating that endoglin is needed in vivo for TGFbeta1 signaling during extraembryonic vascular development. In addition, we have observed cardiac defects in homozygous endoglin-deficient embryos, suggesting endoglin also plays a role in cardiogenesis. We anticipate that heterozygous mice will ultimately serve as a useful disease model for HHT1, as some individuals have dilated and fragile blood vessels similar to vascular malformations seen in HHT patients.

Animals↗
PubMedDate not supplied

Sarcoplasmic reticulum membrane and heart development.

Intracellular Ca2+ concentrations in cardiac cells are dependent on trans-sarcolemmal Ca2+ fluxes and the ability of sarcoplasmic reticulum to release and take up Ca2+. Ca2+ accumulation by sarcoplasmic reticulum membranes causes muscle to relax, whereas Ca2+ release from sarcoplasmic reticulum initiates contraction. Ca2+ transport by the sarcoplasmic is mediated by a Ca2+-dependent ATPase enzyme. Ca2+ release from sarcoplasmic reticulum may be mediated by a ligant-gated Ca2+ channel. The physiological role of sarcoplasmic reticulum in developing muscle is not well established. In this report we investigated the composition and function of sarcoplasmic reticulum membranes during cardiac myogenesis. Phospholamban, a major phosphoprotein in mature sarcoplasmic reticulum membranes was present during early stages of cardiac myogenesis. The embryonic form of phospholamban was phosphorylated by cAMP-dependent protein kinase but not in the presence of Ca2+ and calmodulin. Ca2+ uptake and Ca2+-dependent ATPase activity were low in fetal sarcoplasmic reticulum compared to adult control membranes, although the apparent affinities of the enzyme for Ca2+ were similar. Sarcoplasmic reticulum vesicles used in these studies had very low levels of plasma membrane and mitochondrial contamination. The amounts of both 110-kDa Ca2+-ATPase and 55-kDa calsequestrin in the sarcoplasmic reticulum membrane were lower in fetal sarcoplasmic reticulum vesicles compared to mature membranes. Ca2+-ATPase and calsequestrin were identified in the isolated sarcoplasmic reticulum vesicles using specific antibodies produced against these membrane proteins. Age-related differences in Ca2+ transport properties of cardiac sarcoplasmic reticulum and in the amount of Ca2+-ATPase and calsequestrin may explain alterations in the regulation of intracellular Ca2+ concentrations in fetal heart muscle. This may relate to the developmental changes observed in myocardial function.

Adenosine Triphosphatases↗
PubMed2006

Oct-3/4 dose dependently regulates specification of embryonic stem cells toward a cardiac lineage and early heart development.

The transcriptional mechanisms underlying lineage specification and differentiation of embryonic stem (ES) cells remain elusive. Oct-3/4 (POU5f1) is one of the earliest transcription factors expressed in the embryo. Both the pluripotency and the fate of ES cells depend upon a tight control of Oct-3/4 expression. We report that transgene- or TGFbeta-induced increase in Oct-3/4 mRNA and protein levels in undifferentiated ES cells and at early stages of differentiation triggers expression of mesodermal and cardiac specific genes through Smad2/4. cDNA antisense- and siRNA-mediated inhibition of upregulation of Oct-3/4 in ES cells prevent their specification toward the mesoderm and their differentiation into cardiomyocytes. Similarly, Oct-3/4 siRNA injected in the inner cell mass of blastocysts impairs cardiogenesis in early embryos. Thus, quantitative Oct-3/4 expression is regulated by a morphogen, pointing to a pivotal and physiological function of the POU factor in mesodermal and cardiac commitments of ES cells and of the epiblast.

Animals↗
PubMed1990

[Peripubertal longitudinal study by echocardiography of left heart development in a group of ice hockey players].

The modalities of left ventricular (LV) adaptation (dilatation and/or hypertrophy) to exercise are not as well known in children as in adults. Therefore, the authors followed up 11 national ice hockey players, initially aged 10, following an eight hour per week training schedule for a period of 5 years. M mode echocardiographic studies were carried out each year during the training period to measure LV internal dimensions, wall thickness, myocardial mass and contractility (fractional shortening and systolic stress index). The evolution of these parameters was evaluated (Student's test) by two year peripubertal periods (10-12 years: 12-14 years) and compared in absolute values and in rate of growth with the standardised values indexed to body surface area reported by Henry. Between 10 and 12 years of age, the LV internal dimensions (a good indicator of LV volume in healthy children) increased significantly (p less than 0.05) and LV mass increased very significantly (p less than 0.01). The LV internal dimensions were normal at the outset and remained in the upper limits of normality reported by Henry with a normal rate of growth. Myocardial mass was normal at the age of 10 and its rate of growth was also normal. Between 12 and 14 years of age, the increase in LV internal dimensions was not statistically significant but myocardial mass increased very significantly (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1993

Chronic modifications of lung and heart development in glucocorticoid-treated newborn rats exposed to hyperoxia or room air.

We assessed the mechanics and morphology of the lung in 165 rats treated neonatally with either room air (RA), O2, RA + steroids, or O2 + steroids. Newborn Sprague-Dawley male rats were randomly assigned to these groups. O2-exposure (0.96-1.0 FiO2) lasted 5 days, and dexamethasone treatment consisted of eight daily S.C. injections of drug or buffer in successive doses of 0.5, 0.4, 0.3, 0.2, 0.1, 0.1, 0.1, and 0.1 mg/kg. At 58 days, right ventricular systolic pressure (RVP) was measured. At 60 days, all rats were sacrificed for obtaining lung weight and DNA, saline pressure-volume (P-V) curves, and morphometry. We weighted right ventricles (RV) and left ventricles + septa (LV). Hyperoxia alone did not, but steroid decreased survival rate to 79.4% (95.3% in RA rats, P < 0.02). Only 21 of 40 (52%) O2 + steroids rats survived, less than in both RA groups (P < 0.001). RV weight, RVP and muscularization of alveolar duct arteries were significantly increased in O2 vs. RA rats. In RA + steroids rats, weight of the LV was decreased but RV, RVP, and lung vasculature were not affected. These effects were additive in the O2 + steroid group. Wet lung weights and DNA were increased for RA + steroid rats over all others. O2 and steroids shifted the P-V curve to the left and O2 + steroids still further. Maximal lung volume increased significantly with RA + steroids and still further in O2 + steroids but not in O2 alone. O2 and steroids significantly increased the mean linear intercept and O2 + steroids even more so.(ABSTRACT TRUNCATED AT 250 WORDS)

Air↗
PubMed1998

An autocrine function for transforming growth factor (TGF)-beta3 in the transformation of atrioventricular canal endocardium into mesenchyme during chick heart development.

Transformation of atrioventricular canal endocardium into invasive mesenchyme is a critical antecedent of cardiac septation and valvulogenesis. Previous studies by Potts et al. (Proc. Natl. Acad. Sci. USA 88, 1510-1520, 1991) showed that treatment of atrioventricular canal endocardial and myocardial cocultures with TGFbeta3 antisense oligodeoxynucleotides blocked mesenchyme formation. Based on this observation, we sought to: (i) identify the target tissue of TGFbeta3 antisense oligos in this transformation bioassay, and (ii) more clearly define the mechanism of TGFbeta3 function in atrioventricular canal mesenchyme formation. In situ hybridization and immunohistochemistry showed little or no TGFbeta3 mRNA or protein in the atrioventricular canal myocardium or endocardium prior to mesenchyme formation (stage 14; paraformaldehyde fixation). However, by stage 18 transforming atrioventricular canal endocardial cells and mesenchyme as well as myocardium were positive for both TGFbeta3 mRNA and protein. In culture bioassays, atrioventricular canal endocardial monolayers pretreated with antisense phosphorothioate oligodeoxynucleotides to TGFbeta3 did not transform into invasive mesenchyme in response to cardiocyte conditioned medium: the subsequent addition of exogenous TGFbeta3 protein relieved this inhibition. Control cultures without pretreatment or those receiving missense oligos generated similar numbers of invasive mesenchyme in response to cardiocyte conditioned medium. Direct addition of TGFbeta3 protein to atrioventricular canal endocardial monolayers in the absence of cardiocyte conditioned medium resulted in loss of cell:cell associations and stimulated cellular hypertrophy, but did not engender invasive mesenchyme formation or alter endocardial proliferation after 24 h of culture. Similar results were obtained with TGFbeta2 protein, either alone or in combination with TGFbeta3. The results of this study indicate that: (i) atrioventricular canal endocardium expresses TGFbeta3 in response to a myocardially derived signal other than TGFbeta3, (ii) atrioventricular canal endocardial TGFbeta3 functions in an autocrine fashion to elicit selected characteristics necessary for cushion tissue formation, and (iii) TGFbeta3 alone or in combination with TGFbeta2 is insufficient to transform atrioventricular canal endocardium into invasive mesenchyme in culture.

Animals↗
PubMed2002

Functional and molecular characterization of a T-type Ca(2+) channel during fetal and postnatal rat heart development.

T-type calcium current (I(CaT)) is distributed among a large variety of species and tissues. The main functions of I(CaT) are thought to be related to pacemaker activity and to the cell cycle. Using the whole-cell patch-clamp configuration, we showed that fetal rat ventricular cells exhibit an I(CaT) with electrophysiological and pharmacological characteristics similar to those already described for this current. We investigated I(CaT) density and found that this current was mainly expressed in fetal cells and remained stable until birth (3.1+/-0.3 pA/pF for 18-day-old fetus, n=9). I(CaT) density decreased soon after birth (2.0+/-0.3 pA/pF, n=6, 1.1+/-0.2 pA/pF, n=5, for 1- and 5-day-old rats, respectively) and was no longer detected in 21-day-old rats. The rat ventricular cells express an alpha 1H isoform in addition to a homologous alpha 1G variant. Interestingly, the Ni(2+) sensitivity of I(CaT) indicates that in newborn myocytes, I(CaT) is only generated by alpha 1G subunits, whereas both alpha 1G and alpha 1H subunits participate in the fetal I(CaT). Moreover, the relative contribution of each subunit varies during fetal developmental stages, with a major contribution of alpha 1H in 16-day-old fetuses. Through quantitative RT-PCR we showed that the amount of both alpha 1G and alpha 1H transcripts are developmentally regulated. In fetuses of less than 18 days and in newborn rats after 1 day old, the transcriptional levels of alpha 1G and alpha 1H subunits clearly mismatch the functional contribution of these subunits to I(CaT). However, in perinatal period, the amount of alpha 1G mRNA seems to be in accordance to alpha 1G-related I(CaT) density. In conclusion, we showed that I(CaT) is mainly expressed during fetal stages, that alpha 1G and alpha 1H differentially participate to I(CaT) and that alpha 1G and alpha 1H isoforms are regulated by both transcriptional and post-transcriptional mechanisms.

Amino Acid Sequence↗
PubMed1996

Differential expression of C-protein isoforms in the developing heart of normal and cardiac lethal mutant axolotls (Ambystoma mexicanum).

Regulated assembly of contractile proteins into sarcomeric structures, such as A- and I-bands, is still currently being defined. The presence of distinct isoforms of several muscle proteins suggests a possible mechanism by which myocytes regulate assembly during myofibrillogenesis. Of several muscle isoforms located within the A-band, myosin binding proteins (MyBP) are reported to be involved in the regulation and stabilization of thick filaments during sarcomere assembly. The present confocal study characterizes the expression of one of these myosin binding proteins, C-protein (MyBP-C) in wild-type and cardiac lethal mutant embryos of the axolotl, Ambystoma mexicanum. C-protein isoforms are also detected in distinct temporal patterns in whole-mounted heart tubes and thoracic skeletal muscles. Confocal analysis of axolotl embryos shows both cardiac and skeletal muscles to regulate the expression of C-protein isoforms over a specific developmental window. Although the CPROAxslow isoform is present during the initial heartbeat stage, its expression is not retained in the adult heart. C-protein isoforms are simultaneously expressed in both cardiac and skeletal muscle during embryogenesis.

Ambystoma↗
PubMed2002

Non-radioactive in situ detection of mRNA in ES cell-derived cardiomyocytes and in the developing heart.

Non-radioactive in situ hybridisation is an excellent method to visualise mRNA molecules within their topographical context. Recently we have reported a new non-radioactive in situ hybridisation procedure on tissue sections that is essentially based on the whole mount in situ hybridisation procedure. This method is superior in spatial resolution and sensitivity compared to the radioactive in situ hybridisation procedure. Generally, low levels of gene expression, such as found with the developmental onset of gene expression and in differentiating embryonic stem cells, are difficult to detect by in situ hybridisation. Here an application of the protocol is presented which is based on tyramide signal amplification, which enables the detection of very low abundant mRNAs. The significance of this method is two-fold: (1) the molecular phenotype of embryonic stem cell-derived cardiomyocytes can be examined at the cellular level with high sensitivity, and (2) the number of cells that express the gene of interest can be assessed.

Animals↗
PubMed1993

Identification of DNA-binding protein(s) in the developing heart.

An antiserum (anti-H2) directed at the second helix of the helix-loop-helix (HLH) protein MyoD1 reacts with a protein expressed during avian cardiac myocyte differentiation. Indirect immunohistochemical whole mount staining with anti-H2 detected a protein expressed in stage 11 hearts, but not in hearts of older embryos. At the cellular level, this staining is confined to the nucleus of cardiac cells suggesting that these proteins may have DNA-binding abilities. Several proteins were immunoprecipitated by anti-H2 from stage 11 heart tissue. Protein extracts from similarly staged hearts, when incubated with the muscle-specific enhancer sequence of muscle creatinine kinase (MCK), gave a stage-specific band shift in electromobility shift assays (EMSA), and these protein-DNA complexes were recognized and supershifted by anti-H2. Incubation with a MCK sequence containing a mutated E box did not produce a shift. The specific shift was present as early as stage 6, remained through stage 13, and disappeared by stage 17. These data suggest the presence of at least one protein that is transiently expressed in the differentiating cardiac myocyte, that is immunochemically reactive with an antiserum raised against the second helix of MyoD1, and that binds to a muscle-specific DNA enhancer sequence.

Amino Acid Sequence↗
PubMedDate not supplied

Decoding the language of the heart: developing a physiology of inclusion.

Constructs such as homeostasis and fight/flight have supported a scientific approach to physiology that has yielded a vast database of obvious heuristic value. Yet in spite of its value, these constructs have tended to create a mind-set that unwittingly supports what this article has labeled a "physiology of exclusion." Reinforced by the philosophy of René Descartes, this perspective has led investigators to focus on isolated or separate animal organisms that are reflexively wired for self-preservation. It has created a mind-set in which both research investigators and the public at large tend to view the human body as either in a steady state of vigilance, maximally prepared for fight/flight, or in a state of quiescence. Assumptions of the solitary body, and solitary man wired to react for "self" preservation, has made it difficult to incorporate a growing body of evidence that indicates that social support and loving relationships are conducive to good health. It also has made it difficult for investigators to fully understand why human loneliness is a major cause of premature death. This article delineates these trends and offers a new construct, one that suggests that a "physiology of inclusion" be added to the prevailing view of a "physiology of exclusion." Recent cardiovascular research is cited to help underscore the potential heuristic value of this new physiological construct.

Aggression↗
PubMed2002

Fetal echocardiography: a window to the developing heart.

This paper aims to help the reader understand the indications and the underlying physiologic concepts that relate to the findings obtained from a fetal cardiac evaluation. Techniques to obtain the basic fetal echocardiographic views and to identify gross cardiac abnormalities will also be discussed.

Echocardiography↗