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At least 1,153 records · Page 64Linked to original sources
PubMed2003

Spatiotemporal pattern of commitment to slowed proliferation in the embryonic mouse heart indicates progressive differentiation of the cardiac conduction system.

Patterns of DNA synthesis in the developing mouse heart between ED7.5-18.5 were studied by a combination of thymidine and bromodeoxyuridine labeling techniques. From earliest stages, we found zones of slow myocyte proliferation at both the venous and arterial poles of the heart, as well as in the atrioventricular region. The labeling index was distinctly higher in nonmyocardial populations (endocardium, epicardium, and cardiac cushions). Ventricular trabeculae showed lower proliferative activity than the ventricular compact layer after their appearance at ED9.5. Low labeling was observed in the pectinate muscles of the atria from ED11.5. The His bundle, bundle branches, and Purkinje fiber network likewise were distinguished by their lack of labeling. Thymidine birthdating (label dilution) showed that the cells in these emerging components of the cardiac conduction system terminally differentiated between ED8.5-13.5. These patterns of slowed proliferation correlate well with those in other species, and can serve as a useful marker for the forming conduction system.

Animals↗
PubMed2004

Expression of bone morphogenetic protein-10 mRNA during chicken heart development.

In this communication we describe the expression pattern of BMP10 mRNA during cardiac development in chickens. BMP10 is considered an important factor in the regulation of cardiac growth and trabeculation in the murine embryo. We identified chicken Ests, which are similar to mouse and human BMP10 in the UMIST database. The cDNA clone that contained most sequences was obtained, verified by sequence analysis, and used to determine the spatiotemporal pattern of gene expression. BMP10 mRNA is initially expressed at HH10 in the myocardium of the arterial pole of the heart tube, anterior to the interventricular groove. Between HH14 and HH22, BMP10 mRNA becomes broadly expressed in the outflow tract, the distal part of the inflow tract, and the trabeculated part of the developing ventricles and atria. From HH31 onward, BMP10 mRNA expression decreases in the ventricular myocardium by first disappearing from the compact myocardium and then from the tips of the trabecules. At HH44, BMP10 mRNA is expressed only in the trabeculated myocardium of the atria and the endocardium of the ventricles. The observed expression pattern of BMP10 mRNA suggests that it may play a role in regulating the formation of the ventricular wall and trabecules.

Animals↗
PubMed2005

Normal distribution of melanocytes in the mouse heart.

We report the consistent distribution of a population of pigmented trp-1-positive cells in several important septal and valvular structures of the normal mouse (C57BL/6) heart. The pigmented cell population was first apparent by E16.5 p.c. in the right atrial wall and extended into the atrium along the interatrial septum. By E17.5, these cells were found along the apical membranous interventricular septum near or below the surface of the endocardium. The most striking distribution of dark pigmented cells was found in the tricuspid and mitral valvular leaflets and chordae tendineae. The normal distribution of pigmented cells in the valvuloseptal apparatus of C57BL/6 adult heart suggests that a premelanocytic lineage may participate in the earlier morphogenesis of the valve leaflets and chordae tendineae. The origin of the premelanocyte lineage is currently unknown. The most likely candidate populations include the neural crest and the epicardially derived cells. The only cell type in the heart previously shown to form melanocytes is the neural crest. The presence of neural crest cells, but not melanocytes, in some of the regions we describe has been reported by others. However, previous reports have not shown a contribution of melanocytes or neural crest derivatives to the atrioventricular valve leaflets or chordae tendineae in mouse hearts. If these cells are of neural crest origin, it would suggest a possibly greater contribution and persistence of neural crest cells to the valvuloseptal apparatus than has been previously understood.

Animals↗
PubMed2006

Heuristic problems in defining the three-dimensional arrangement of the ventricular myocytes.

There is lack of consensus concerning the three-dimensional arrangement of the myocytes within the ventricular muscle masses. Bioengineers are seeking to model the structure of the heart. Although the success of such models depends on the accuracy of the anatomic evidence, most of them have been based on concepts that are far from anatomical reality, which ignore many significant previous accounts of anatomy presented over the past 400 years. During the 19th century, Pettigrew emphasized that the heart was built on the basis of a modified blood vessel rather than in the form of skeletal muscles. This fact was reemphasized by Lev and Simkins as well as Grant in the 20th century, but the caveats listed by these authors have been ignored by proponents of two current concepts, which state either that the myocardium is arranged in the form of a "unique myocardial band," or that the walls of the ventricles are sequestrated in uniform fashion by laminar sheets of fibrous tissue extending from epicardium to endocardium. These two concepts are themselves incompatible and are further at variance with the majority of anatomic studies, which have emphasized the regional heterogeneity to be found in the three-dimensional packing of the myocytes within a supporting matrix of fibrous tissue. We reemphasize the significance of this three-dimensional muscular mesh, showing how the presence of intruding aggregates of myocytes extending in oblique transmural fashion also contends against the notion that all myocytes are orientated with their long axes parallel to the epicardial and enodcardial surfaces.

Animals↗
PubMed1978

Calcification in an intramyocardial mass lesion: isolated calcification of an accessory papillary muscle in a patient with mitral prolapse.

Cardiac catheterization in a 50-year-old male with mitral leaflet prolapsed revealed a filling defect with calcification in the high posterolateral wall. At surgery, the lesion was found to be a calcified accessory papillary muscle with thickened, calcified chordae to the posterior leaflet. The calcification and fibrosis were felt to be due to friction lesions between elongated chordae and the endocardium. Intracardiac calcification in mitral leaflet prolapsed may suggest calcified mitral apparatus.

Calcinosis↗
PubMed1990

Temporary cardiac pacing using a new, steerable, balloon-tipped pacing catheter.

A new balloon-tipped, flow-directed, steerable pacing catheter for unipolar temporary ventricular pacing is presented. It was successfully and uneventfully tested in 25 patients with acute myocardial infarction in the coronary care unit. The main advantage of the new catheter is the ease with which a stable contact may be achieved between the pacing electrode and the endocardium.

Arrhythmias, Cardiac↗
PubMed1991

Transseptal left heart catheterization: usefulness of the intracavitary electrocardiogram in the localization of the fossa ovalis.

One of the major difficulties in left heart catheterization through the interatrial septum is to ensure that the Brockenbrough needle tip is correctly laid on the fossa ovalis floor (FOF), which is the only area where the puncture must be done. The difficulties may be enhanced in patients with atrial enlargement and subsequent distortion of the anatomical structures. In order to reduce the hazards of the septal puncture, an electrocardiographic mapping of the right atrial endocardium was performed using the Brockenbrough needle as an exploratory electrode in a group of 20 patients. When the tip of the needle was laid against the FOF, the endoatrial electrocardiogram (EAE) registered a slight or no injury curve, even when the pressure was tight enough to perforate the septum. On the contrary, the pressure on any other area of the muscular septum or atrial walls elicited a bizarre monophasic injury curve. The peculiar electrocardiographic response of the FOF to the pressure exerted by the Brockenbrough needle tip was a valuable aid to identify the area where the transseptal puncture must be done. In addition, the sudden changes in the P wave morphology immediately after the septal perforation, provided the first clue that the left atrium has been reached.

Animals↗
PubMed1984

Abnormal left ventricular filling in patients with sustained myocardial relaxation: assessment of diastolic parameters using radionuclide angiography and echocardiography.

Parameters of left ventricular filling obtained from time-activity curves of radionuclide angiograms were compared with parameters of myocardial relaxation from digitized M-mode curves of the free wall endocardium in 25 consecutive patients. Eight patients had normal left ventricular systolic and diastolic function. Five patients with low ejection fraction (EF less than 50%) also had abnormal values of peak filling rate (PFR), time to peak filling rate (Tr), and/or time constant of endocardial retraction (Te). Twelve patients with normal EF had three (40%), two (40%), or one (20%) of the diastolic parameters within the pathological range. Tr correlated significantly with Te (r = 0.88, p less than 0.001), and patients with Te prolongation always had high values of Tr. One of the diastolic parameters (PFR) correlated significantly with EF (r = 0.60, p less than 0.01). Parameters of left ventricular filling and myocardial relaxation are thus abnormal in many patients with normal systolic function, indicating that diastolic parameters may be more sensitive to myocardial deterioration.

Adult↗
PubMed1988

Diagnostic accuracy of 2-D echocardiography for detection of exercise-induced wall motion abnormalities in patients with coronary artery disease: comparison to biplane cineventriculography.

To determine the accuracy of two-dimensional echocardiography (2-D echo) for assessment of exercise-induced wall motion abnormalities in patients with coronary artery disease, the results of stress echocardiography were compared with exercise cineventriculography. In 56 consecutive patients, biplane cineventriculography at rest and immediately after supine bicycle exercise was performed. Cross-sectional echo was obtained using the apical two- and four-chamber-views for left ventricular imaging under identical conditions. In 6 of the 56 patients 2-D echo, in 8 patients cineventriculogram, and in 2 patients both methods were of inadequate quality at rest or during exercise. Of the remaining 40 patients, 34 had coronary artery disease. Local wall motion in 360 wall segments from these patients was analyzed. In 49 segments (14%) in 24 of these patients exercise-induced ischemic wall motion abnormalities were evident during cineventriculography. Only 24 of these 49 asynergies (49%) were also recognized by 2-D echo. Using cross-sectional echocardiography, ischemia-related wall motion abnormalities were best detected septal, whereas apical asynergies were identified in only 3 of 12 segments (25%). Thus, the clinical value of exercise 2-D echo as a screening method in patients suspected of having coronary artery disease is limited and restricted to patients where excellent visualization of the left ventricular endocardium is possible.

Cineangiography↗
PubMed1998

Streptococcal mural endocarditis and myocardial abscess occurring in a left ventricular aneurysm--case report and review.

Infection of the mural endocardium within a left ventricular aneurysm without valvular involvement is exceedingly rare. The presenting clinical features can be non-specific, and a high index of suspicion is required for its diagnosis. Delay in diagnosis invariably leads to a fatal outcome. Although no controlled studies are available to guide therapy and management of these patients, appropriate antibiotic therapy and early surgical resection of the infected ventricular aneurysm remain the cornerstone of therapy.

Aneurysm, Infected↗
PubMed2003

Germ-line transmission of a myocardium-specific GFP transgene reveals critical regulatory elements in the cardiac myosin light chain 2 promoter of zebrafish.

In response to the lack of a transgenic line of zebrafish labeled with heart-specific fluorescence in vivo to serve as a research model, we cloned a 1.6-kb polymerase chain reaction (PCR) -product containing the upstream sequence (-870 bp), exon 1 (39 bp), intron 1 (682 bp), and exon 2 (69 bp) of the zebrafish cardiac myosin light chain 2 gene, (cmlc2). A germ-line transmitted zebrafish possessing a green fluorescent heart was generated by injecting this PCR product fused with the green fluorescent protein (GFP) gene with ends consisting of inverted terminal repeats of an adeno-associated virus. Green fluorescence was intensively and specifically expressed in the myocardial cells located both around the heart chambers and the atrioventricular canal. Neither the epicardium nor the endocardium showed fluorescent signals. The GFP expression in the transgenic line faithfully recapitulated with the spatial and temporal expression of the endogenous cmlc2. Promoter analysis showed that the fragment consisting of nucleotides from -210 to 34 (-210/34) was sufficient to drive heart-specific expression, with a -210/-73 motif as a basal promoter and a -210/-174 motif as an element involved in suppressing ectopic (nonheart) expression. Interestingly, a germ-line of zebrafish whose GFP appeared ectopically in all muscle types (heart, skeletal, and smooth) was generated by injecting the fragment including a single nucleotide mutation from G to A at -119, evidence that A at -119 combined with neighboring nucleotides to create a consensus sequence for binding myocyte-specific enhancer factor-2.

Adenoviridae↗
PubMed2001

Coexpression of endothelial PAS protein 1 with essential angiogenic factors suggests its involvement in human vascular development.

Endothelial PAS protein 1 (EPAS1) is a bHLH-PAS transcription factor involved in cellular response to hypoxia. Its precise role in angiogenesis is unclear, but several genes essential to vascular development, including those encoding vascular endothelial growth factor (VEGF), its receptor VEGFR-2 and Tie2, are thought to be targets of EPAS1. To investigate whether this transcription factor and its putative targets were expressed concomitantly, we performed in situ hybridization on serial adjacent sections of human embryos at gestational ages of 3 to 6 weeks. We studied expression of the genes encoding EPAS1, VEGF, VEGFR-1, and -2, Tie2, and its ligands, angiopoietin (Ang) 1 and 2. We also compared these expression profiles with that of hypoxia-inducible factor 1alpha (HIF1alpha). EPAS1 transcripts were detected in several types of endothelial cell: in blood vessels walls, the endocardium, the glomeruli of the mesonephros, and the sinusoids of the liver. In these endothelial cells, expression of EPAS1 systematically or partly coincided with Tie2 and the VEGF receptors expression. There was also some overlap between the sites of synthesis of EPAS1 and VEGF mRNAs, principally in hepatocytes and sympathetic ganglion cells. In addition, we found that EPAS1 and HIF1alpha transcripts were often colocalized, suggesting a functional redundancy of these two transcription factors during development. These observations are consistent with transactivation by EPAS1 of the expression of its putative target genes during embryogenesis, suggesting that this transcription factor is involved in human angiogenesis. They provide evidence that EPAS1 is involved in the regulation of vascular maturation, remodeling, or stabilization rather than in the early steps of embryonic angiogenesis.

Angiogenesis Inducing Agents↗
PubMed2004

Popeye domain containing gene 2 (Popdc2) is a myocyte-specific differentiation marker during chick heart development.

The Popeye domain containing (popdc) genes constitute a novel gene family encoding proteins of the plasma membrane in muscle cells, with three N-terminal transmembrane domains and a cytoplasmic carboxy terminus. In vertebrates, three members of the Popdc gene family have been described. However, in the chick system only two cDNAs, Popdc1 and Popdc3, have been cloned previously. By screening a chick expressed sequence tag database, we report here the identification of five alternatively spliced chick Popdc2 cDNAs with different carboxy termini. Northern blot analysis revealed expression of Popdc2 predominantly in the myocardium and weaker expression in skeletal muscle. By whole-mount in situ hybridization, chick Popdc2 was first detected at Hamburger and Hamilton (HH) stage 7 within the anterior part of the heart fields. In the tubular heart, atrial and ventricular precursor cells stained positively for Popdc2. Weaker expression was observed in myocardium of the outflow tract and sinus venosus. By HH stage 18, the outer curvature myocardium was strongly stained, whereas expression in myocardium of the inner curvature was negligible. Popdc2 expression was absent from the endocardium and propepicardial organ. At HH stage 36, Popdc2 expression was confined to the compact layer myocardium. In addition to the heart, Popdc2 expression was also observed in the myotome and in the muscle-forming fields of the limbs. Our results indicate that Popdc2 is highly expressed in the developing heart and may serve as a novel marker of myocardial differentiation in the chick embryo.

Alternative Splicing↗
PubMed2004

Expression of VE-cadherin in zebrafish embryos: a new tool to evaluate vascular development.

We have identified the zebrafish homologue of VE-cadherin and documented its expression in the developing vascular system. The zebrafish VE-cadherin gene is specifically expressed in the vascular endothelial cell lineage beginning with the differentiation and migration of angioblasts and persists throughout vasculogenesis, angiogenesis, and endocardium development. Staining zebrafish embryos by whole-mount in situ hybridization with the VE-cadherin probe provides a method to screen embryos for vascular defects. To illustrate this utility, we used VE-cadherin expression to demonstrate a conservation of vascular endothelial growth factor-A (VEGF-A) function. The morpholino antisense oligonucleotide knockdown of VEGF-A function in zebrafish embryos results in a loss of angiogenic blood vessels, as indicated by the lack of VE-cadherin expression in the intersegmental vasculature. This loss can be restored in embryos supplemented with either zebrafish or human VEGF-A, the latter indicating that genes crucial to angiogenesis have highly conserved functional activities in vertebrates.

Amino Acid Sequence↗
PubMed2006

Mesp1-nonexpressing cells contribute to the ventricular cardiac conduction system.

Previous fate mapping analysis, using Cre recombinase driven by the Mesp1 locus, revealed that Mesp1 is expressed in almost all of the precursors of the cardiovascular system, including the endothelium, endocardium, myocardium, and epicardium. Mesp1-nonexpressing cells were found to be restricted to the outflow tract cushion and along the interventricular septum (IVS), which is a location that is suggestive of specialized cardiac conduction system (CCS). In our current study, we examined the identity of these IVS cells by using the pattern of beta-galactosidase activity in CCS-lacZ mice. In addition, by crossing Mesp1-Cre and floxed GFP reporter mice with CCS-lacZ mice, we have calculated that approximately 20% of the ventricular CCS within the IVS corresponds to Mesp1-nonexpressing cells. These data suggest that the ventricular CCS is of heterocellular origin. Furthermore, we indicate a possibility that a population of the cells that contribute to the ventricular CCS might be distinguished at an early stage of development.

Animals↗
PubMed2006

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

The proteoglycan versican is essential to the formation of endocardial cushion mesenchyme by epithelial-mesenchymal transformation (EMT). A potentially important factor in the regulation of versican activity during cushion EMT is proteolysis by ADAMTS metalloproteinases. Using antibodies to the DPEAAE neoepitope created by ADAMTS proteolysis of versican, we detected the amino terminal 70-kDa versican cleavage fragment in cardiac cushions. Initially (i.e., 9.5 days post coitum [dpc]), the fragment is associated with endocardial cells undergoing EMT and with newly derived mesenchymal cells. ADAMTS-1 and its cofactor fibulin-1 were also associated with these cells. As cushions become increasingly populated with mesenchymal cells (10.5-12.5 dpc), the fragment remains asymmetrically distributed compared with the pattern of total versican. Highest levels of the fragment are present in regions immediately subjacent to the endocardium characterized as having densely packed, rounded cells, lacking cellular protrusions. With further development (i.e., 12.5-14.5 dpc), the pattern of fragment distribution within cushions broadens to include the ECM surrounding loosely packed mesenchymal cells in the cushion core. Together, the findings reveal that versican proteolysis leading to the production of the 70-kDa fragment is integral to the formation and differentiation of endocardial cushion mesenchyme.

ADAM Proteins↗
PubMed2006

MEKK4 regulates developmental EMT in the embryonic heart.

Congenital heart malformations occur at a rate of one per one hundred births and are considered the most frequent birth defects. This high incidence of cardiac defects underscores the complex developmental processes required to form the first functioning organ in mammals. The molecular cues which govern heart development are poorly defined and require an improved understanding in order to advance repair strategies for heart defects. The cytoplasmic MAP kinase kinase kinase, MEKK4, is a critical effector in cellular stress responses; however, the function of MEKK4 during embryonic development and cardiogenesis is not well understood. We have identified MEKK4 as a critical signaling molecule during cardiovascular development. We report the detection of MEKK4 transcripts to early myocardium, endocardium and to cardiac cushion cells that have executed epithelial to mesenchymal transformation (EMT). These observations suggest that MEKK4 may function during production of the cushion mesenchyme as required to create valves and the septated heart. We used a kinase inactive form of MEKK4(MEKK4(KI)) in an in vitro assay that recapitulates in vivo EMT, and show that MEKK4(KI) attenuates mesenchyme production. However, addition of a constitutively active MEKK4 into ventricular explants, a system that does not normally undergo EMT, is not able to cause mesenchymal cell outgrowth. Thus, the kinase activity of MEKK4 is essential, but not sufficient, to support developmental EMT. This knowledge provides a basis to understand how MEKK4 may integrate signaling cascades controlling heart development.

Animals↗
PubMed2005

Prenatal sonographic features of isolated hypoplastic left heart syndrome.

Hypoplastic left heart syndrome (HLHS) is a spectrum of fetal conditions associated with severe hypoplasia of the left ventricle and left ventricular outflow tract. The purpose of this series was to focus on the sonographic prenatal features of isolated HLHS. Based on the 5 cases presented here, the prenatal sonographic features of HLHS include small-sized left ventricle, atretic or hypoplastic mitral valves with restricted motion and a small amount of antegrade flow or regurgitation, and hypoplastic ascending aorta. Retrograde flow in the transverse aortic arch strongly suggests inadequate systemic output from the left heart. Tricuspid regurgitation is common and increases the chance for the development of hydrops. Other findings may be helpful, including left ventricular hyperechoic endocardium and increased nuchal translucency at 11-14 weeks. With careful fetal echocardiography, HLHS may be readily observed on a 4-chamber view as either a small or even absent left ventricle.

Abortion, Eugenic↗