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PubMed1999

Multiple developmental roles of VEGF suggested by a LacZ-tagged allele.

Vascular endothelial growth factor (VEGF) is an angiogenic factor and a potent stimulator of microvascular permeability. It is a mitogen specific for endothelial cells. The expression of VEGF and its two receptors, Flk-1 and Flt-1, is pivotal for the proper formation of blood vessels in embryogenesis as shown by gene-targeting experiments. Interestingly, the loss of even a single allele of VEGF led to embryonic lethality between day E9.5 and day E10.5 in the mouse. To assess the role of VEGF during embryonic development we decided to tag VEGF expression with LacZ, by inserting an IRES (internal ribosome entry site)-LacZ reporter cassette into the 3' untranslated region of the gene. This alteration enabled us to monitor VEGF expression throughout embryonic development at single-cell resolution. beta-Galactosidase expression from the altered VEGF locus was first observed prior to gastrulation and was detectable at all stages of vascular development in the embryo. Later, the specific cellular distribution and the level of VEGF expression indicated its pleiotropic role in development. High expression levels seemed to be associated with vasculogenesis and permeability, whereas lower levels were associated with angiogenesis and cell migration. In addition, we found VEGF expression in a subtype of endothelial cells present in the endocardium. We believe that the LacZ-tagged allele we have generated offers a precise means of detecting VEGF expression under a variety of physiological and pathological conditions.

Alleles↗
PubMed1999

Receptor-type protein-tyrosine phosphatase mu is expressed in specific vascular endothelial beds in vivo.

We investigated the localization of receptor-type protein-tyrosine phosphatase mu (RPTPmu) in tissues by immunofluorescence. RPTPmu immunoreactivity was found almost exclusively within vascular endothelial cells. RPTPmu was more abundant in the arterial tree than in the venous circulation. This pattern of expression was opposite to that of the von Willebrand factor and demonstrated a lack of difference in expression of VE-cadherin. RPTPmu was undetectable in the endocardium. In agreement with previous work on nonendothelial cell lines, RPTPmu was exclusively at the lateral aspects of endothelial cells in vivo and at cell-cell contacts as well as ex vivo in two- or three-dimensional endothelial cell cultures, and expression levels were upregulated by cell density. RPTPmu was detected in few other cells: bronchial and biliary epithelia and cardiocytes (intercalated discs). Our results identify RPTPmu as a new marker of endothelial cell heterogeneity and suggest a possible role in endothelial-specific functions, involving cell-cell contact.

Animals↗
PubMed1996

Transmural changes in stress-free myocyte morphology during pressure overload hypertrophy in the rat.

Cellular hypertrophy can alter the distribution of residual stress in the myocardium, hence can affect active and passive ventricular mechanics. It is hypothesized that an increase in stress-free cell cross-sectional area will tend to increase residual stresses. Therefore transmural distributions of myocyte cross-sectional areas and global ventricular dimensions in young rats 0-21 days following thoracic aortic handling with sham-operated and unoperated control groups were measured in tissue free of all external and residual stresses. Cell cross-sectional area increased in the stress-free state and was uniform across the wall except at 21 days when there was a transmural gradient with cells at the endocardium 46% larger in diameter than those in the outer wall. Cell area increased from a mean of 156 +/- 30 microM2 at 0 days to a mean of 627 +/- 164 microM2 at 21 days, although during this time there were no statistical changes in the opening angles of stress-free tissue sections. Because the time course of opening angle did not follow the changes in cell thickening, the cellular growth measured in this study is probably not the only factor responsible for the distribution of residual stress.

Analysis of Variance↗
PubMed1997

Resting tension participates in the modulation of active tension in isolated guinea pig ventricular myocytes.

We studied active and passive properties of intact isolated guinea-pig ventricular myocytes in auxotonic conditions. Cells were attached using carbon fibres. The passive properties of the myocytes, in the presence of the stretch-activated channel blocker streptomycin sulphate, could be separated into two groups: stiff cells (stiffness slope = 2.88 +/- 0.93 nN/micron3, n = 63 cells) and compliant cells (stiffness slope = 0.91 +/- 0.35 nN/micron3, n = 52 cells). The study and the localization of the different kind of cells indicated that endocardium is mainly constituted of stiff cells (80%) while the epicardium contained more compliant cells (60%). When a longitudinal strain was applied to compliant cells, an increase in resting tension, diastolic sarcomere length and active tension were observed. On the other hand, in stiff cells, it induced an increase in resting tension and active tension with little change of diastolic sarcomere length. In both kinds of cells, strain had no effect on Ca2+ transient amplitude and shape. Plotting active tension v diastolic sarcomere length also clearly showed two separated populations of cells, corresponding to stiff and compliant cells. The results of the two groups of cells when plotting active tension v resting tension could not be distinguished. We conclude that resting tension is an important factor in the modulation of active tension by stretch in addition to interfilament lattice spacing or sarcomere length.

Animals↗
PubMed1997

Regulation of expression of the [3H]-dofetilide binding site associated with the delayed rectifier K+ channel by dexamethasone in neonatal mouse ventricle.

Developmental shortening of cardiac action potential duration in mouse appears to result, at least in part, from replacement of the rapid component of the delayed rectifying potassium current (IKr) with the transient outward current (ItO1). This developmental decrease in the IKr current density was paralleled by a loss of the high affinity [3H]-dofetilide binding site and loss of prolongation of action potential duration by dofetilide. Since glucocorticoid treatment prevented the developmental shortening of action potential duration in rats in the perinatal period, we hypothesized that chronic dexamethasone treatment would alter the developmental loss of IKr channel expression in mice. Accordingly, 10-day-old mice were randomly allocated to chronic in vivo dexamethasone treatment (1 mg/kg) or placebo treatment for 3-5 days. At 15 days of life, transmembrane action potentials were recorded in right ventricular endocardium and [3H]-dofetilide equilibrium binding studies were performed. The baseline action potential duration in the dexamethasone-treated animals was significantly greater than that in the control group (66+/-3 v 54+/-10 ms, respectively; P<0.01). Moreover, dofetilide significantly prolonged action potential duration in the dexamethasone-treated animals, but had no effect on the placebo-treated group (P<0.01). In addition, a high affinity [3H]-dofetilide binding site (Kd 96+/-21 nM and Bmax 69+/-13 fmoles/mg protein) was observed in the dexamethasone-treated group (n=5), whereas no specific [3H]-dofetilide binding was observed in the placebo-treated group. In conclusion, dexamethasone modulates developmental regulation of IKr channel expression in mouse ventricle.

Action Potentials↗
PubMed1997

Localization of alpha1(I) collagen mRNA in myocardium from the spontaneously hypertensive rat during the transition from compensated hypertrophy to failure.

Spontaneously hypertensive rats (SHR) commonly develop impairment of myocardial function between ages 18-24 months. Isolated muscle studies demonstrate depressed myocardial contractility and increased passive stiffness. Studies of the extracellular matrix in SHR with failure (SHR-F) demonstrate an increased expression of genes encoding extracellular matrix components (ECM), hydroxyproline concentration and fibrosis relative to age-matched non-failing animals. In the present study, tissue sections of hearts from SHR-F, non-failing SHR (SHR-NF) and non-hypertensive Wistar Kyoto rats (WKY) were hybridized with a cDNA probe for alpha1(I) collagen mRNA, which was found by Northern blot analysis to be elevated in SHR-F relative to hearts from control animals. In situ hybridization studies demonstrate increased perivascular and interstitial collagen alpha1(I) gene expression in myocardium from the SHR relative to WKY. In addition, failing hearts from the SHR demonstrate focal alpha1(I) collagen mRNA accumulation in the endocardium and at sites of degenerating single myocardial cells.

Animals↗
PubMed1997

Study of microcirculation by coloured microspheres and NMR-microscopy in isolated rat heart: effect of ischaemia, endothelin-1 and endothelin-1 antagonist BQ 610.

Although the investigation of coronary microcirculation is of great importance, available methods have severe restrictions. They do not allow the study of vasodynamics of resistance vessels and microscopic conductance vessels simultaneously in the isolated beating rat heart. We now demonstrate that the combined measurement of perfusion which reflects the state of resistance vessels and cross-sections of microscopic conductance vessels is feasible in the model of the isolated constant flow perfused rat heart. Perfusion measurement was based on injection of coloured microspheres. Cross-sections of microscopic conductance vessels (diameter >140 micron) were determined by NMR-microscopy by flow weighted imaging. Both methods were established recently by our group. The combined measurement was applied to hearts which were subjected to ischaemia and reperfusion (group 1: n=5, 15 min ischaemia/group 2: n=7, 30 min ischaemia/measurements before ischaemia and 15/30 min after reperfusion), 200 pmol endothelin-1 bolus application (group 3: n=6/measurements before and 5 min after drug application), continuous infusion of the endothelin-1 antagonist BQ 610 (group 4: n=6/measurements before and 20 min after onset of infusion), and 200 pmol endothelin-1 application superimposed on 20 min of continuous BQ 610 infusion (group 5: n=7/combined measurement before BQ 610 infusion and 5 min after endothelin-1 application). In group 1, 15 min reperfusion restored the pre-ischaemic perfusion state, whereas conductance vessels were dilated (80.8+/-2.6%), after 30 min reperfusion pre-ischaemic conditions were also restored for conductance vessels. In group 2, a redistribution of perfusion from left ventricular endocardium to the right ventricular wall was observed. Post-ischaemic rhythm disturbances made NMR-imaging in this group impossible. In group 3, a shift of perfusion from the left ventricular myocardium to the right ventricular wall was observed. Similarly, the cross-section of left ventricular conductance vessels decreased (-32.6+/-2.1%), whereas size of right ventricular vessels increased. In group 4, BQ 610 had no effect on perfusion nor on vessel size and antagonized the effect of endothelin-1 on perfusion and vessel size in group 5.

Animals↗
PubMed1998

Angiotensin II, transforming growth factor-beta1 and repair in the infarcted heart.

Tissue repair following myocardial infarction (MI) eventuates in fibrous tissue formation at the site of myocyte necrosis. Following a large transmural MI, fibrosis appears remote to the infarct site. This is associated with extensive tissue remodeling that adversely affects ventricular diastolic function. Substances involved in promoting fibrous tissue formation at MI and remote sites are under investigation. Angiotensin II (AngII), generated at sites of repair, has been implicated. However, its regulatory role on fibrous tissue formation remains uncertain. In the present study we sought to determine whether AngII is correlated to transforming growth factor beta 1 (TGF-beta1) expression, a regulator of fibrous tissue formation, at these sites of tissue repair. We studied: (1) localization and expression of angiotensin converting enzyme (ACE), AngII receptors, TGF-beta1 mRNA and its receptors in the infarcted rat heart; and (2) effect of AngII on TGF-beta1 synthesis by chronic blockade of AT1 receptors began at the time of surgery by losartan in rats with MI. Hearts were studied at 4 weeks post-MI. We found: (1) low-density ACE, AngII and TGF-beta1 receptor binding and low mRNA for type I collagen and TGF-beta1 in the normal heart; (2) fibrosis at sites of MI and remote to it, including endocardium and fibrosis of intraventricular septum, interstitial fibrosis of non-infarcted myocardium and fibrosis of visceral pericardium; (3) markedly increased (P<0.01) and colocalized ACE, AngII and TGF-beta1 receptor binding, type I collagen and TGF-beta1 mRNA at MI and remote sites of repair; (4) increased TGF-beta1 concentration (P<0. 01) at these sites; and (5) attenuated TGF-beta1 and type I collagen gene expression (P<0.01) at these sites in rats receiving losartan. These observations suggest locally generated AngII via ATi receptor binding is correlated to TGF-beta1 expression and synthesis at sites of repair and remote sites in the infarcted rat heart. The mechanism responsible for the role of AngII in TGF-beta1 remains to be elucidated.

Angiotensin II↗
PubMed1999

Developmental regulation of the translational repressor NAT1 during cardiac development.

The process of translation initiation has been postulated to play an important role in the regulation of cellular growth and proliferation. Here, we report the identification and differential expression of a fundamental translational repressor NAT1, during early postnatal cardiac development. Differential display analysis of RNA obtained from 3-day and 4-week-old rat hearts resulted in the cloning and identification of a 396 bp cDNA fragment (DRCF-6) which corresponded to the 3' terminal portion of NAT1. Northern blot analysis revealed that the mRNA expression of NAT1 was markedly elevated during the first 2 weeks of postnatal life, with an apparent peak level of expression occurring at 1 week. NAT1 mRNA levels then steadily decreased to 4 weeks of age. The NAT1 transcript has previously been shown to be extensively edited by the enzyme APOBEC-1, which deaminates specific cytidine bases to uridine; cytidine deamination at a glutamine codon (CAA) results in the formation of a stop codon (UAA) and consequently, premature termination of translation. Accordingly, Western blot analysis detected the presence of several smaller proteins in addition to the full length NAT1 protein (97 kDa), each exhibiting a distinct pattern of expression during cardiac development. APOBEC-1 editing of NAT1 during cardiac development was further supported by primer extension analysis of cytidine 1699, which was found to be predominantly edited to uridine. Immunohistochemical staining showed that NAT1 is expressed predominantly in atrial and ventricular myocytes, although staining was also detected in vascular smooth muscle cells and in the endocardium. These results suggest that NAT1 may play a role in the postnatal development of the heart and demonstrate that APOBEC-1 editing may possibly be a novel mechanism by which translation is regulated during cardiac development.

Aging↗
PubMed2001

Renin expression at sites of repair in the infarcted rat heart.

Y. Sun, J. Zhang, J. Q. Zhang and K. T. Weber. Renin Expression at Sites of Repair in the Infarcted Rat Heart. Journal of Molecular and Cellular Cardiology (2001) 33, 995-1003. Angiotensin (Ang) II has autocrine and paracrine functions that contribute to structural cardiac remodeling by fibrous tissue following myocardial infarction (MI). The recruitment of angiotensin converting enzyme (ACE) and AngII receptors by inflammatory and fibroblast-like cells involved in tissue repair of the infarcted heart is now well established. On the other hand, the temporal and spatial response and cellular source of renin in infarcted hearts have not been fully elucidated. The relationship between renin synthesis and circulating renin activity have likewise not been addressed. The present study sought to assess the cellular source, spatial distribution and temporal response of renin expression and synthesis in the rat heart following anterior transmural MI, and to determine its relationship to circulating renin activity. At day 3 and weeks 1, 2, 3 and 4 following left coronary artery ligation, the localization and optical density of cardiac renin mRNA was detected by quantitative in situ hybridization; cardiac and circulating renin activity was measured by radioimmunoassay; cells expressing cardiac renin were detected by immunohistochemistry; and injury/repair was assessed by hematoxylin/eosin and collagen-specific picrosirius red staining. Unoperated rats served as normal controls. The authors found: (1) renin mRNA and activity were not detected in either normal control or non-infarcted myocardium, but were expressed at the site of infarction and other sites of repair involving visceral pericardium and endocardium of interventricular septum at all time points; (2) cells expressing renin at day 3 and weeks 1 and 2 were predominantly macrophages, while at weeks 3 and 4, they were primarily myofibroblasts; (3) renin activity in the infarcted myocardium rose progressively over the course of 4 weeks; and (4) circulating renin activity was significantly increased at day 3 and week 1, reached a peak at week 2, declined at week 3 and returned to normal levels at week 4. Thus, renin expression and activity appear at sites of repair in the infarcted rat heart on day 3 and rise progressively thereafter over 4 weeks, independent of circulating renin. Several types of cells are responsible for renin synthesis at these sites; primarily macrophages during the inflammatory phase of repair, and myofibroblasts during the subsequent fibrogenic phase. Cardiac renin production following MI contributes to local AngII generation that regulates tissue repair and structural remodeling following MI.

Actins↗
PubMed1999

Dynamics of intramural scroll waves in three-dimensional continuous myocardium with rotational anisotropy.

It has been suggested that reentrant activity in three-dimensional cardiac muscle may be organized as a scroll wave rotating around a singularity line called the filament. Experimental studies indicate that filaments are often concealed inside the ventricular wall and consequently, scroll waves do not manifest reentrant activity on the surface. Here we analyse how such concealed scroll waves are affected by a twisted anisotropy resulting from rotation of layers of muscle fibers inside the ventricular wall. We used a computer model of a ventricular slab (15x15x15 mm(3)) with a fiber twist of 120 degrees from endocardium to epicardium. The action potential was simulated using FitzHugh-Nagumo equations. Scroll waves with rectilinear filaments were initiated at various depths of the slab and at different angles with respect to fiber orientation. The analysis shows that independent of initial conditions, after a certain transitional period, the filament aligns with the local fiber orientation. The alignment of the filament is determined by the directional variations in cell coupling due to fiber rotation and by boundary conditions. Our findings provide a mechanistic explanation for the prevalence of intramural reentry over transmural reentry during polymorphic ventricular tachycardia and fibrillation.

Action Potentials↗
PubMed1995

Transmural distribution of capillary morphology as a function of coronary perfusion pressure in the resting canine heart.

Changes in coronary perfusion pressure lead to alterations in intracoronary myocardial volume that may be associated with regionally altered microvascular morphology. Transmural variations in coronary capillary geometry were quantified as a function of coronary perfusion pressure in glutaraldehyde-fixed canine hearts. Capillary volume fractions, diameter, numerical density, anisotropy, and sarcomere length were measured using computer analysis of light microscopic images of sections taken transverse or longitudinal to the muscle fiber axis. Capillary volume was 4-6% of myocardial wall volume and exhibited a significant transmural gradient, increasing from epicardium to endocardium. Vessels 4 to 5 microns in diameter with a density of 2900 mm-2 appear to increase in diameter and alter their cross-sectional shape with increasing pressure, rather than increasing in number, suggesting an effective distensibility of approximately 0.007 mm Hg-1. Quantification of vessel anisotropy was directly related to cross-sectional shape and demonstrated that the capillaries are highly oriented. These findings indicate that intramyocardial capacitance is at least in part associated with nonhomogeneous changes in coronary capillary morphology with altered perfusion pressure.

Animals↗
PubMed1999

GATA transcription factors and cardiac development.

Three members of the GATA family of transcription factors, GATA-4, -5, and -6, are expressed in the developing heart. One family member, GATA-5, is restricted to the endocardium while the other two, GATA-4 and -6, are present in the myocardium where they apparently fulfil distinct functions. The mechanisms underlying GATA factor specificity are not fully understood but may involve interaction with other tissue-restricted or ubiquitous co-factors. Thus, combinatorial interaction among GATA factors or between GATA factors and other co-factors may differentially control various stages of cardiogenesis.

Animals↗
PubMed1994

Immunohistochemical localization of CYP1A and CYP3A-like isozymes in hepatic and extrahepatic tissues of Atlantic cod (Gadus morhua L.), a marine fish.

The cellular localization of inducible CYP1A and constitutive CYP3A-like forms in different organ systems of Atlantic cod (Gadus morhua) was determined in control fish and fish exposed to beta-naphthoflavone (BNF). Paraffin-embedded sections were stained with polyclonal rabbit anti-cod P450 1A IgG or rabbit anti-rainbow trout P450con (a putative CYP3A form which cross-reacts with purified cod P450b) serum by the avidin-biotin peroxidase complex method. Following BNF-exposure of cod, CYP1A induction was immunohistochemically demonstrated in hepatocytes and endothelial cells of liver, the endocardium and vascular endothelium in the atrium and ventricle, and epithelial cells of the proximal tubular segment, endothelial cells, and interrenal cells in kidney. The vascular endothelium was the main site of induction of CYP1A in gills, spleen, gut, pyloric caecae, and gonads. The CYP3A-like isozyme P450b was mainly localized to hepatocytes, renal tubular epithelium, and epithelial cells of the mucosa in the intestine. Furthermore, the distribution of P450b was not affected by BNF exposure. The localization of P450b bears interesting similarities to the localization of CYP3A in mammals supporting the CYP3A-like identity of cod P450b. Simultaneous localization of inducible CYP1A and a constitutively expressed CYP isoenzyme has not previously been reported in fish. This is also the first presentation of cellular distribution of a CYP3-like isozyme in fish. Staining of CYP1A in endothelial cells supports previous observations that endothelium is a major site of CYP1A induction following xenobiotic exposure in fish. The observation of CYP1A induction in interrenal cells has important implications for possible endocrine effects of xenobiotic exposure.

Animals↗
PubMed1997

Expression of the aryl hydrocarbon receptor (AhR) and AhR nuclear translocator during chick cardiogenesis is consistent with 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced heart defects.

We examined cardiotoxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the chick embryo and the cardiac expression of transcription factors, the aryl hydrocarbon receptor (AhR) which binds TCDD, and its dimer partner, the AhR nuclear translocator (Arnt). Chicken eggs were injected with control (triolein) or 1.0 pmol TCDD/g egg prior to incubation and collected on Day 10 when cardiomorphogenesis is complete. Relative to controls, TCDD increased heart wet weight (27.2 +/- 0.5 versus 36.6 +/- 1.3 mg, p < 0.001) and dry weight (2.7 +/- 0.1 versus 3.1 +/- 0.1 mg, p < 0.01), and tended to increase heart myosin content (3.5 +/- 0.6 versus 6.3 +/- 2.5 microg, p < 0.07), suggesting an increase in cardiac muscle mass and edema. Histologic and morphometric analyses revealed that 10/13 TCDD-exposed hearts exhibited enlarged right and left ventricles, thickened ventricular septum, and a thinner left ventricular wall with increased trabeculation, and 4/13 exhibited ventricular septal defects compared to controls (0/23). To evaluate AhR and Arnt expression, untreated chick embryos were collected on Days 2.2, 3, 4, 5, and 8 of incubation, preserved in Bouin's fixative, sectioned, and stained with AhR and Arnt antibodies. The AhR was expressed ubiquitously in cardiac myocytes, while Arnt expression was restricted to myocytes overlying developing septa: atrioventricular canal, outflow tract, and atrial and ventricular septa. Both proteins were absent from endocardium and endocardial-derived mesenchyme. In addition, cardiac expression of an AhR/Arnt target, cytochrome P4501A1, was restricted to myocardium coexpressing AhR and Arnt. Thus, the spatial and temporal expression of AhR and Arnt suggests that the developing myocardium and cardiac septa are potential targets of TCDD-induced teratogenicity, and such targets are also consistent with cardiac hypertrophy and septal defects observed following TCDD exposure.

Animals↗
PubMed1999

Transcriptional activation of avian CYP1A4 and CYP1A5 by 2,3,7, 8-tetrachlorodibenzo-p-dioxin: differences in gene expression and regulation compared to mammalian CYP1A1 and CYP1A2.

The toxicity, carcinogenicity, and biochemical effects of 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) are dependent upon activation of the Ah receptor, a ligand-activated transcription factor. Ah receptor activation leads to the induction of cytochrome P450 (CYP) 1A enzymes, which include CYP1A1 and 1A2 in mammals and CYP1A4 and 1A5 in chickens. CYP1A induction is a major effect of TCDD exposure although its relationship to TCDD toxicity and carcinogenicity are not understood. In these studies we investigated by nuclear run-on transcription assays along with Northern and Western blotting in chick embryo liver, kidney, and heart whether avian CYP1A4 and 1A5, like mammalian CYP1A1 and 1A2, are transcriptionally induced by TCDD and whether the chick CYP1A enzymes exhibit differences analogous to mammalian CYP1A enzymes in organ expression. We report that CYP1A4 and 1A5, like CYP1A1 and 1A2, are transcriptionally induced by TCDD in liver. However, whereas CYP1A1 is not constitutively expressed in liver, CYP1A2 and both CYP1A4 and 1A5 are constitutively expressed. Further, whereas TCDD induces only CYP1A1 and not CYP1A2 in extrahepatic organs, TCDD induces both CYP1A4 and 1A5 in chick kidney. Also, TCDD induced CYP1A4 but not 1A5 in both myocardium and heart vessels whereas CYP1A1 induction has only been found in endocardium. Further, liver CYP1A4 and 1A5 mRNAs had the same half lives and were both superinduced by cycloheximide, whereas mRNA half lives differ for CYP1A1 and 1A2, and cycloheximide superinduces only CYP1A1. We suggest that there are species differences in the effects of TCDD on CYP1A gene expression, organ distribution, and regulation that are likely to be accompanied by differences in CYP1A function and that this diversity may contribute to the large differences in sensitivity to TCDD among species.

Animals↗
PubMed1975

Relations between development of the capillary wall and myoarchitecture of the rat heart.

The type of the blood supply to the myocardium appears to be closely related to its structural arrangement. The heart of adult poikilotherm animals is either entirely spongious, supplied from the ventricular cavity or its spongious musculature is covered by an outer compact layer with vascular supply. The size of the compact layer increases with increasing heart weight. The changes in the heart size during the ontogenetic development of honoiotherms are accompanied by the gradual transformation of the vascularless spongious musculature into a compact myocardium supplied thrugh coronary vessels. Up to the development of coronary arteries (in the rat up to the 17th day of embryonic life - ed) the myocardium is entirely spongious and supplied from mentricular cavity. Two types of primitive vascular bed are characteristic for this period: a) intertrabecular spaces, which penetrate deep into the ventricular wall as direct continuation of the endocardium, and b) intramyocardial clefts without endothelial lining. During further development of the terminal mascular bed, the outgrowth of endothelial cells into the myocardial clefts is important. The first capillaries with closed endothelial wall can be observed on the 18th ed. At this time various developmental stages o the terminal blood bed can be observed simultaneously. Within the following period (20-21 ed) the thick capillary walls become narrow and pericytes occur. The process of differentiation spreads in both ventricles and in septum from the base to the cardiac apex and is practically finished by the 14th day of postnatal life. The longitudinal orientations of myofibres starts between the 20th and 22nd ed. The final arrangement of muscle cells and capillaries into three layers (outer and inner longitudinal, central circular) is terminated during the second postnatal week.

Animals↗
PubMed1993

The distribution and characterization of HNK-1 antigens in the developing avian heart.

The heart originates from splanchnic mesoderm and to a lesser extent from neural crest cells. The HNK-1 monoclonal antibody is a marker for early migrating neural crest cells, but reacts also with structures which are not derived from the neural crest. We investigated whether heart structures are HNK-1 positive before neural crest cells colonize these target tissues. To that end, we determined the HNK-1 antigen expression in the developing avian heart on immunohistochemical sections and on Western blots. The HNK-1 immunoreactivity in the developing chick heart is compared with data from literature on the localization of neural crest cells in chick/quail chimeras. Structures with neural crest contribution, including parts of the early outflow tract and the related endocardial cushions, the primordia of the semilunar valve leaflets and the aorticopulmonary septum were HNK-1 positive. Furthermore, other structures were HNK-1 positive, such as the atrioventricular cushions, the wall of the sinus venosus at stage HH 15 through 21, parts of the endocardium at E3, parts of the myocardium at E6, and the extracellular matrix in the myocardial base of the semilunar valves at E14. HNK-1 expression was particularly observed in morphologically dynamic regions such as the developing valves, the outflow tract cushion, the developing conduction system and the autonomic nervous system of the heart. We observed that atrioventricular endocardial cushions are HNK-1 positive. We conclude that: a HNK-1 immunoreactivity does not always coincide with the presence of neural crest cells or their derivatives; (2) the outflow tract cushions and atrioventricular endocardial cushions are HNK-1 positive before neural crest cells are expected (stage HH 19) to enter the endocardial cushions of the outflow tract; (3) the observed spatio-temporal HNK-1 patterns observed in the developing heart correspond with various HNK-1 antigens. Apart from a constant pattern of HNK-1 antigens during development, stage-dependent HNK-1 antigens were also found.

Animals↗