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PubMed1996

Coronary vascularization during development in the rat and its relationship to basic fibroblast growth factor.

OBJECTIVE: Our overall aims were to elucidate the temporal and spatial sequence of coronary vascularization during development in the rat, and to determine whether basic fibroblast growth factor expression corresponds to any phase of the vascularization process. METHODS: Immunohistochemical, histochemical, morphometric and in situ hybridization analyses were performed on prenatal and postnatal hearts of various ages. RESULTS: Coronary vascularization, which begins at embryonic day 13 (E13) with blood island-like structures in the epicardium, progresses from this layer toward the endocardium as indicated by a transmural gradient of vascular volume throughout the ventricles. Vascular smooth muscle first appears in E17 hearts at the time a capillary-like plexus coalesces and penetrates the aorta to form the main coronary arteries. These vessels maintain an anastomatic morphology and must undergo subsequent remodeling in order to assume adult branching characteristics. The early postnatal period is characterized by development of the arterial tree and the enzymatic differentiation of the arteriolar and venular ends of the capillary bed. Although bFGF is expressed both prenatally and postnatally, the highest mRNA expression was noted during the early period of vascularization (E14 and E15), and the early neonatal period (1-6 days) which corresponds to a period of substantial microvascular growth. CONCLUSIONS: Coronary vascularization follows a temporal sequence which includes transmural expansion of the capillary bed, arteriolar formation subsequent to vascular penetration of the aorta, and postnatal growth, differentiation, and remodeling. Since high levels of bFGF expression are correlated with key time points in coronary vascular growth, bFGF may play an important role in this process.

Alkaline Phosphatase↗
PubMed1996

Inhibition of outflow cushion mesenchyme formation in retinoic acid-induced complete transposition of the great arteries.

OBJECTIVE: Endocardial cushion tissue formation, the primordia of valves and septa, is a critical event in cardiac morphogenesis. Maternally administrated all-trans retinoic acid is known to induce complete transposition of the great arteries (TGA) in the mouse embryo. To address the mechanisms of TGA, the effect of retinoic acid on cushion tissue formation was examined. METHODS: Using a three-dimensional collagen gel culture model, we performed various types of endothelial-mesenchymal transformation assays of co-cultured endocardium with myocardium obtained from 9.5-day mouse embryonic hearts. In vivo immunohistochemical detections of extracellular matrices, fibronectin and type I collagen, were also performed. RESULTS: Endothelial-to-mesenchymal transformation at the onset of cushion tissue formation was suppressed in the outflow tract of embryos exposed to retinoic acid in culture. This inhibitory effect of retinoic acid was spatially restricted to the outflow tract and reversed by treatment with embryonic myocardial conditioned medium enriched in extracellular inductive molecules. Mesenchyme formation in the outflow tract was inhibited at a lower concentration of retinoic acid (10(-10) mol/l) than that which inhibited the atrio-ventricular canal (10(-7) mol/l) in culture. The fibronectin and type I collagen depositions in pre-migratory outflow tract cardiac jelly in retinoic acid-treated embryonic heart were reduced compared to those in the control. CONCLUSIONS: Exogenously applied retinoic acid inhibits outflow tract cushion mesenchyme formation in the embryonic heart with TGA. It is suggested that retinoic acid inhibits the expression of extracellular matrices and inductive molecules synthesized by myocardium in the outflow tract.

Animals↗
PubMed1977

[Experimental study of successive range of excitation of the heart ventricles].

The succession of excitation spreading about the cardiac ventricles was studied in 28 dogs using the intramural multipolar technique. The primary foci of excitation were found in the zones of the subendocardium on the borderline between the lower and middle portions of the left side of the ventricular septum, and under the base of the anterior papillary muscle on the right side of the ventricular septum. The excitation of the interventricular septum throughout its thickness occurs first of all in the anterior part of its mid-portion where the depolarization waves moves exclusively from left to right. Lastly the posterior lateral subendocardial layers of the bases of the free walls and the upper portion of the ventricular septum are depolarized. In some parts of the interventricular septum and of the left free wall the excitation wave first reaches the zones located deeply under the endocardium, then spreads towards the endo- and epicardium, changing its direction several times.

Action Potentials↗
PubMed1997

Absence of endocardial lymphoid infiltrates (Quilty lesions) in nonheart transplant recipients treated with cyclosporine.

The clinical records and autopsy material from 14 patients treated with cyclosporine who were not recipients of cardiac allografts were reviewed to further study the nature of endocardial lymphoid infiltrates (quilty lesions). Although there was well-documented exposure to cyclosporine, no endocardial lymphoid infiltrates were identified in these cases, providing evidence that the endocardial-based Quilty lesion is not the result of the direct effect of cyclosporine and may represent a localized form of heart rejection confined to the endocardium.

Adolescent↗
PubMed1997

[Comparison of myocardial velocities by tissue color Doppler imaging in normal subjects and in dilated cardiomyopathy].

The authors studied 35 normal subjects (41 +/- 6 years) and 22 patients with idiopathic dilated cardiomyopathy 48 +/- 7 years; ejection fraction: 31 +/- 12%) in order to determine normal values of myocardial velocities and to demonstrate the sensitivity of Doppler tissue imaging in detecting a significant decrease in myocardial velocities in patients with abnormal left ventricular contractility. Interventricular septal and left ventricular posterior wall velocities were recorded by M mode long axis parasternal views. In normal subjects, a velocity gradient in the posterior wall was observed, higher in the endocardium than in epicardium, in systole (5.1 +/- 1.5 versus 2.8 +/- 1 cm/s, p < 0.01), and early diastole (13.7 +/- 3.5 versus 5.7 +/- 2 cm/s, p < 0.001) and late diastole at the time of atrial contraction (2.7 +/- 2.1 versus 1.8 +/- 1.7 cm/s, p < 0.01). Moreover, the velocities are higher in the posterior wall than in the interventricular septum throughout the cardiac cycle. Finally, the velocities are higher in early diastole than in systole, both in the interventricular septum and posterior wall. In the group of patients with idiopathic dilated cardiomyopathy, the intramyocardial velocities were lower than in normal subjects. In addition, the velocity gradient in the posterior wall was absent in 15 of the 22 patients. The authors conclude that Doppler tissue imaging provides new information in the analysis of myocardial function both in systole and diastole.

Adolescent↗
PubMed1998

[Experimental endocarditis. Pathological anatomy of human endocarditis].

Experimental reproduction of human endocarditis in animal models has been based on the induction of structural lesions in valve endocardium using different methods. The primary lesion caused in this way is the so called non-bacterial thrombotic endocarditis. Its colonization is then induced by inoculation of microorganisms in the bloodstream. Freedman's modified method has been the most widespread model of this type. It has mainly been performed in rabbits with inoculation of Staphylococcus aureus or alpha-hemolitic Streptococcus. Experimental models of endocarditis have contributed to our knowledge of the pathogenic mechanisms, causative agents and predisposing factors of endocarditis. They have also allowed us to develop appropriate diagnostic, therapeutic and prophylactic measures for its management.

Animals↗
PubMed1998

[Measurement of the left ventricular mass using MRI with automatic determination of the endocardial and epicardial contours].

This study describes a method of automatic border detection of the left ventricular endocardium and epicardium associating three methods of segmentation (increase of region, border detection and adaptive threshold), applicable to the evaluation of ventricular mass and volume by magnetic resonance imaging. Despite slight underestimation, the spin-echo sequence used in 9 small pigs provided a value of left ventricular mass close to that observed ex vivo (r = 0.97, SEE = 6.05 g). Clinical validation using a rapid gradient-echo sequence was undertaken and compared with manual border detection carried out by three independent, trained operators. The study population included healthy subjects and patients with global or segmental left ventricular dysfunction with or without ventricular deformation. The correlations between automatic and manual detection were satisfactory both for calculation of left ventricular mass (r = 0.93, SEE = 13 g) and measurement of surfaces (r = 0.91, SEE = 1.4 cm2). The concordance of the two methods was confirmed by the Bland and Altman test. Cardiac magnetic resonance imaging may provide accurate and reproducible measurements of left ventricular mass within acceptable acquisition and image processing times for routine use. Although the clinical value of such a method is accepted both for establishing the prognosis and guiding management, studies of the cost/efficacy ratio should be undertaken to situate magnetic resonance imaging with respect to other non-invasive techniques of investigation of left ventricular function.

Adult↗
PubMed1996

Latent transforming growth factor-beta is present in the extracellular matrix of embryonic hearts in situ.

Transforming growth factor-beta (TGF-beta) is an important regulator of development. In vitro, TGF-beta is secreted in a latent, inactive form and can be activated by pH extremes, chaotropic agents, or cell-surface proteases. However, there is little evidence for the existence of latent TGF-beta in vivo. In this study, we determined whether (1) cultured embryonic cardiac segments secrete latent or active TGF-beta, (2) binding of TGF-beta antibody to TGF-beta was conformation-dependent (i.e., active vs. latent), and (3) immunostaining of embryonic hearts changed after exposure to activating conditions. Only latent TGF-beta 3 (acid activatable) was detected in conditioned medium of stage 14-16 chick cardiac segments as measured by a growth inhibition bioassay. No growth-inhibitory activity was present in nonacidified control medium. When blotted onto a membrane, only transiently acidified conditioned medium bound TGF-beta antibody. These data showed that cardiac segments secrete latent TGF-beta which binds with antibody if activated. To determine if antibody binding to tissue sections required exposure to TGF-beta-activating conditions, stage 14-16 embryos were fixed and sectioned under conditions that maximally retained extracellular matrix (ECM). Under these conditions, immunostaining was found in the myocardium but not in the endocardium or cardiac ECM. Limited immunostaining was found in other areas of the embryo and was always cell-associated. In addition to the above staining, when tissue sections were exposed to TGF-beta activating conditions, immunopositive staining was present within most of the embryonic ECM including the cardiac ECM. All immunostaining was blocked by preabsorption with TGF-beta 3 protein. These data suggest that active TGF-beta has a very limited distribution while latent TGF-beta is more abundant in embryonic ECM. Therefore, in vivo activation of TGF-beta may play an important role in mediating the expression of TGF-beta function during development.

Animals↗
PubMed1996

Expression of the beta 4 integrin subunit in the mouse heart during embryonic development: retinoic acid advances beta 4 expression.

Using immunohistochemical techniques as well as in situ hybridization we were able to elicit the expression pattern of the beta 4 integrin subunit in the murine heart during development. We show that beta 4 is not expressed in the heart before E13 and is afterwards restricted to the endocardium of the atrioventricular canal, the outflow tract, and the venous valves in the right atrium. As these are all sites of high shear stress in the heart, we propose a role for alpha 6 beta 4 in the tight adhesion of the endocardial cells to their basement membranes in these segments. Moreover, mouse embryos were treated with all-trans retinoic acid, which was previously shown to induce congenital malformations, among which malformations of the heart. We show an advanced expression without ectopic localization of cardiac beta 4 after the administration of retinoic acid. This advanced appearance of beta 4 was also shown in extracardiac tissue like migrating neural crest cells. Several hypotheses on the mechanism of beta 4 up-regulation and a possible role for alpha 6 beta 4 in the development of heart malformations after the administration of retinoic acid are discussed.

Animals↗
PubMed1996

Distinct alpha 7A beta 1 and alpha 7B beta 1 integrin expression patterns during mouse development: alpha 7A is restricted to skeletal muscle but alpha 7B is expressed in striated muscle, vasculature, and nervous system.

The laminin binding alpha 7 beta 1 integrin has been described as a major integrin in skeletal muscle. The RNA coding for the cytoplasmic domain of alpha 7 integrin undergoes alternative splicing to generate two major forms, denoted alpha 7A and alpha 7B. In the current paper, we have examined the developmental expression patterns of the alpha 7A and alpha 7B splice variants in the mouse. The alpha 7 integrin expression is compared to that of the nonintegrin laminin receptor dystroglycan and to that of laminin-alpha 1 and laminin-alpha 2 chains. Alpha 7A integrin was found by in situ hybridization to be specific to skeletal muscle. Antibodies specific for alpha 7B integrin and in situ hybridization revealed the presence of alpha 7 mRNA and alpha 7B protein in the E10 myotome and later in primary and secondary myotubes. In the heart, alpha 7B integrin was not detectable in the endocardium or myocardium during embryonic and fetal heart development. Northern blot analysis and immunohistochemistry revealed a postnatal induction of alpha 7B in the myocardium. In addition to striated muscle, alpha 7B integrin was localized to previously unreported nonmuscle locations such as a subset of vascular endothelia and restricted sites in the nervous system. Comparison of the alpha 7 integrin expression pattern with that of different laminin isoforms and dystroglycan revealed a coordinated temporal expression of dystroglycan, alpha 7 integrin, and laminin-alpha 2, but not laminin-alpha 1, in the forming skeletal muscle. We conclude that the alpha 7A and alpha 7B integrin variants are expressed in a developmentally regulated, tissue-specific pattern suggesting different functions for the two splice forms.

Animals↗
PubMed1997

Spatial and temporal expression of the 72-kDa type IV collagenase (MMP-2) correlates with development and differentiation of valves in the embryonic avian heart.

Extracellular proteases may play an important role in the regulation of cell migration and remodeling of the extracellular matrix during development. In this study, we have examined the embryonic avian heart for the expression of matrix metalloproteases. The 72-kDa type IV collagenase, MMP-2, was detected in extracts of whole hearts and showed a modest increase in amount over time. This increase in enzyme activity corresponded to a small increase in the steady-state level of mRNA for this enzyme. A more dramatic increase was seen in the amount of the 66-kDa activated form of this enzyme as development progressed, suggesting that the process of activation, rather than enzyme synthesis, may be the important regulatory step in this system. Coincident with the change in the level of active MMP-2 was a significant increase in the expression of the MMP-2 activator, MT-MMP, between stages 12 and 24. The message for MMP-2 was expressed by the endocardium of the cushion tissues which was undergoing an epithelial-mesenchymal transition, and by the migrating mesenchymal cells, suggesting a role for this protease in regulating cell motility and matrix invasion. In older staged hearts, the cells of the differentiating valves expressed high levels of MMP-2 which may be important for the final remodeling events in this region.

Animals↗
PubMed1997

Neovascularization of the Xenopus embryo.

The receptor tyrosine kinase, Flk-1 or VEGFR-2, and its ligand, vascular endothelial growth factor (VEGF) are required for the development of the embryonic vasculature. Targeted disruption of either gene in mice results in the failure of vascular system formation. The Xenopus homologues of flk-1 and VEGF have been cloned and their expression has been examined throughout early embryonic development. These studies indicate that flk-1 is expressed in groups of endothelial precursor cells which will form the major blood vessels of the embryo, including the posterior cardinal veins, the dorsal aorta, the vitelline veins, and the endocardium. VEGF expression is found in tissues adjacent to the mesenchyme containing the flk-1-expressing endothelial precursors. Expression of both flk-1 and VEGF is transient, appearing as the primary vascular plexus is forming and declining steadily after the onset of functional embryonic circulation. After establishment of the primary vascular structures, flk-1 expression is also observed in the intersegmental veins which form by an angiogenic mechanism. Overall, these results support a role for VEGF/flk-1 signaling in both vasculogenesis and angiogenesis in the Xenopus embryo. When VEGF is expressed ectopically in Xenopus embryos by microinjection of either plasmid DNA or synthetic mRNA, large, disorganized vascular structures are produced. This result indicates that ectopic VEGF is capable of altering the architecture of the developing vascular network.

Amino Acid Sequence↗
PubMed1998

Chicken winged-helix transcription factor cFKH-1 prefigures axial and appendicular skeletal structures during chicken embryogenesis.

The cDNA cFKH-1 encodes a chicken winged helix/forkhead domain transcription factor that presents a dynamic expression pattern during chicken embryogenesis. Transcripts accumulate predominantly in early paraxial mesoderm, developing somites, and within mesenchymal precursors of skeletal structures. cFKH-1 RNA is first detected in the developing mesoderm of HH stage 6 embryos. During subsequent development cFKH-1 RNA accumulates in a dorsal domain of the anterior presomitic mesoderm and later in all cells of the epithelial somites before it becomes limited to the sclerotome when somites compartmentalise. cFKH-1 expression persists in the sclerotome, forming the vertebrae and in mesenchymal condensations in limb buds that will give rise later to the appendicular bones. In differentiated chondrocytes and definitive bone structures, however, cFKH-1 expression is down-regulated. Additional expression domains are found in mesenchyme of branchial arches and the head, in the dorsal aorta, and weakly in the endocardium. Based on its expression pattern and the structure of the forkhead DNA-binding domain cFKH-1 constitutes a chicken relative to the murine family of fkh-1/MF1 and MFH-1 factors. The embryonic expression of the cFKH-1 gene defines distinct mesodermal domains and suggests that it may regulate gene expression in mesenchymal cell lineages that will form cartilage in trunk and limb buds.

Amino Acid Sequence↗
PubMed1999

Hepatocyte growth factor expression in the developing myocardium: evidence for a role in the regulation of the mesenchymal cell phenotype and urokinase expression.

During development of the heart, the endocardium of the developing cushion tissue transforms into mesenchymal cells that rapidly invade the underlying extracellular matrix. This invasive process, along with subsequent proliferation and differentiation of the mesenchyme, are essential for the normal formation of valvular and septal structures. Several factors have been identified that appear to initiate and/or control this transformation process, including the growth factor TGF-beta. In these studies we have investigated whether hepatocyte growth factor/scatter factor (HGF/SF) may also be involved in some aspects of this transformation process. Using an immunohistochemical approach we have detected a spatially restricted localization of HGF/SF to the myocardial cells of the cushion tissue. HGF was detected in extracts of the developing heart, and the presence of the active form correlated with the onset of the transformation process and the elevation of urokinase activity. The endocardial-derived mesenchymal cells of the cushion tissue were found to express the c-met HGF receptor. Isolated endocardial cells responded to the addition of HGF with increases in motility, proliferation, and urokinase production. The results from these studies suggest that HGF may function as a myocardial-derived mediator of the epithelial-mesenchymal transformation by inducing and/or maintaining the mesenchymal cell phenotype. The increase in urokinase expression by the cushion tissue cells, in response to HGF, may facilitate the invasive abilities of these cells and also provide a means of maintaining high levels of active HGF required for the stimulation of cell proliferation and migration.

Animals↗
PubMed1999

Xl erg: expression pattern and overexpression during development plead for a role in endothelial cell differentiation.

The ets gene family encodes transcription factors related to the proto-oncogene c-ets-1 and involved in cell proliferation, differentiation, and oncogenic transformation. We have characterized the Xenopus homologue of the human erg gene, an ets-related-gene, and its expression has been examined throughout early embryonic development. Xl erg encodes at least two proteins, resulting from alternative splicing events. The transcripts are restricted to the forming endocardium, the endothelial cells of the blood vessels and to the neural crest-derived mesenchyme cells of the pharyngial arches. When Xl ERG is expressed ectopically in Xenopus embryos by microinjection of synthetic mRNA, multiple developmental defects are observed. Dorsally injected embryos have their AP axis shortened and present severe defects in eye and somite morphogenesis. Ventrally injected embryos show a posteriorization of the cells having received the message together with ectopic endothelial cell differentiation as revealed by the accumulation of X-msr transcripts. In both cases, accumulation of erythrocytes in structures not connected with the blood circulatory system can be observed. Our data suggest that Xl erg may be involved in cell motility and in the development of the circulatory system.

Alternative Splicing↗
PubMed2000

Tubedown-1, a novel acetyltransferase associated with blood vessel development.

We have used an embryonic endothelial cell line (IEM cells) as an experimental system for identifying and characterizing new molecules which are regulated during blood vessel development. A novel gene isolated from IEM cells, tubedown-1 (tbdn-1), is expressed at high levels in unstimulated IEM cells and is downregulated during formation of capillary tube structures by the IEM cells induced by basic fibroblast growth factor (bFGF) and leukemia inhibitory factor (LIF) in vitro. Tbdn-1 is also downregulated in M1 myeloid leukemia cells after differentiation in response to LIF in vitro. Tbdn-1 is homologous to the yeast NAT-1 N-terminal acetyltransferases and encodes a novel protein of approximately 69 kDa associated with an acetyltransferase activity. Levels and distribution of tbdn-1 expression are regulated in both endothelial and hematopoietic cells during development in tissues such as the yolk sac blood islands, heart, and liver blood vessels. In the adult, tbdn-1 expression is low or undetected in most organs examined with the exception of the atrial endocardium, the endothelial and myeloid compartments of bone marrow, and the remodeling vascular bed of atretic ovarian follicles. The distribution and regulation of expression of tbdn-1 suggest that this novel acetyltransferase may be involved in regulating vascular and hematopoietic development and physiologic angiogenesis.

Acetyltransferases↗
PubMed1997

Temporal and spatial asymmetries in the initial distribution of mesenchyme cells in the atrioventricular canal cushions of the developing chick heart.

BACKGROUND: We investigated potential early asymmetries in the distribution of mesenchymal cells within the inferior and superior AV cushions in the developing chick heart. METHODS: Chick embryos stages 16-20 HH were fixed, embedded in polyacrylamide, and the cell nuclei stained with propidium iodide. Cells counts were determined within the cardiac jelly of the atrioventricular canal (AV) by laser confocal microscopy in coronal planes spanning its entire length. RESULTS: Our data show at the different stages studied, 16-20 HH, that the inferior AV cushion invariably contains more cells than the superior AV cushion. In the inferior cushion, the cell distribution is bimodal, i.e., the proximal and distal regions have more mesenchymal cells than the middle part of the AV canal. In the superior cushion, there is a increasing gradient of mesenchymal cells along the longitudinal axis from the atrium to the ventricle. CONCLUSIONS: Our findings reveal that the temporal and spatial characteristics of mesenchyme formation in the inferior vs. superior AV cushion are different. This asymmetry suggests several potential hypotheses: (1) the distribution of the inducer molecule or its receptor has a distribution similar to that of mesenchymal cells, (2) the extracellular matrix has a differential composition or regionally-specific physical associations, (3) the endocardium is heterogeneous with respect to transformation capacity, or (4) these patterns result from an earlier inductive event. The potential importance of the observed asymmetries in the distribution of AV mesenchyme is discussed relative to localization patterns of molecules critical to successful cardiac morphogenesis and remodeling.

Animals↗
PubMed1997

Developmental changes in the myocardial architecture of the chick.

BACKGROUND: Numerous studies describing myocardial architecture have been performed on the adult heart but considerably fewer have been made during embryonic or fetal development. To serve as a basis for interspecies comparison of ventricular morphology, and as a reference for studying the effects of experimental perturbations, we examined the development of chick throughout the entire incubation period. METHODS: Chick hearts from stage 14 (day 2) to stage 46 (day 21) were perfusion-fixed, and sectioned in transverse, frontal and sagittal planes. The ventricular myocardial architecture was examined and photographed in the scanning electron microscope. RESULTS: At embryonic stage 16 and earlier, the smooth-walled heart loop had an outer myocardial mantle, cardiac jelly, and endocardium. From stage 18, there was an outer compact and inner trabeculated myocardium. Trabeculated myocardium could be subdivided into the outer (basal) portion adjacent to the compact layer and the central (luminal) part. The outer basal layer could be distinguished from the inner luminal by shorter and finer trabeculae with small, round intertrabecular spaces. From stage 24, the patterns of trabeculae and intertrabecular spaces were ventricle-specific. Between stages 24 to 31, abundant trabeculations were present throughout both ventricular cavities. The trabeculae were initially radially arranged, but later adopted a spiral course, which persisted in a simplified form into adulthood. CONCLUSIONS: The ventricular myocardium undergoes distinctive morphogenesis, characterized by changes in trabecular patterning and orientation. We speculate that the embryonic trabecular architecture reflects the directions of the main stresses. Unlike fetal and adult hearts, which rely mostly on the compact myocardial layer, the trabeculae play a crucial role in the contractile function of the embryonic heart.

Animals↗