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At least 199 records · Page 11Linked to original sources
PubMed1990

Role of sympathetic innervation in cardiac development in oculo.

Embryonic heart cultured in oculo differentiates into adult-like heart tissue, increases in size, and maintains spontaneous activity driven by a defined pacemaker. The growth and beating rate of embryonic heart maturing in oculo are modulated by its neural milieu. Culture in a sympathetically denervated eye chamber compromised growth and increased intrinsic beating rate. Exposure to an additional source of sympathetic neurons increased parasympathetic control of heart rate but did not alter growth or intrinsic beating rate. Because eye chamber sympathectomy alters neurotransmitter expression in parasympathetic and sensory neurons, it is possible that the growth inhibition observed in heart grafts is not a direct consequence of preventing sympathetic innervation. This possibility is being tested in additional experiments.

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PubMed2005

Cytoplasmic thioredoxin reductase is essential for embryogenesis but dispensable for cardiac development.

Two distinct thioredoxin/thioredoxin reductase systems are present in the cytosol and the mitochondria of mammalian cells. Thioredoxins (Txn), the main substrates of thioredoxin reductases (Txnrd), are involved in numerous physiological processes, including cell-cell communication, redox metabolism, proliferation, and apoptosis. To investigate the individual contribution of mitochondrial (Txnrd2) and cytoplasmic (Txnrd1) thioredoxin reductases in vivo, we generated a mouse strain with a conditionally targeted deletion of Txnrd1. We show here that the ubiquitous Cre-mediated inactivation of Txnrd1 leads to early embryonic lethality. Homozygous mutant embryos display severe growth retardation and fail to turn. In accordance with the observed growth impairment in vivo, Txnrd1-deficient embryonic fibroblasts do not proliferate in vitro. In contrast, ex vivo-cultured embryonic Txnrd1-deficient cardiomyocytes are not affected, and mice with a heart-specific inactivation of Txnrd1 develop normally and appear healthy. Our results indicate that Txnrd1 plays an essential role during embryogenesis in most developing tissues except the heart.

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PubMed2003

Three-dimensional reconstruction of gene expression patterns during cardiac development.

The study of the genetic regulation of embryonic development requires the three-dimensional (3D) mapping of gene expression at the microscopic level. Despite the recent burst in the number of methods focusing on 3D reconstruction of embryonic specimens, an adequate and accessible 3D reconstruction protocol for the visualization of patterns of gene expression is lacking. In this communication we describe a protocol that was developed for the 3D visualization of patterns of gene expression determined by in situ hybridization (ISH) on serial sections. The method still requires tissue sectioning, due to penetration limits of the specific staining agents into whole embryo preparations. With regard to expenditure of resources, i.e., hardware, software, and time, the protocol is relatively undemanding. Because the variation between specimens requires the visualization of multiple specimens per stage, it was decided to "do more, less well." The current protocol, therefore, results in reconstructions of sufficient, but not the highest, quality. The use of the protocol is demonstrated on a series of serially sectioned mouse hearts, ranging from embryonic day 8.5 to 14.5. The myocardium of the hearts was identified by ISH using a mixture of specific mRNA probes and reconstructed.

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PubMed2004

Transcription enhancer factor-1-related factor-transgenic mice develop cardiac conduction defects associated with altered connexin phosphorylation.

BACKGROUND: Conduction system defects and slowed ventricular conduction are common in patients with systolic dysfunction and contribute to arrhythmias and sudden death. In animal models of heart failure, cardiac alpha1-adrenergic signaling is constitutively activated. Here, we report the effects of constitutive activation of alpha1-adrenergic signaling on connexin phosphorylation and cardiac conduction. METHODS AND RESULTS: Transgenic mice were generated with cardiac-specific overexpression of the transcription factor RTEF-1 (transcription enhancer factor-1-related factor), which mediates alpha1-adrenergic signaling in cardiac myocytes. Surface and intracardiac ECGs revealed prolongation of the PR, QRS, and AH intervals and the appearance of progressive atrial arrhythmias in RTEF-1 mice. Optical mapping using voltage-sensitive dye revealed slower conduction velocities across the atrial and ventricular myocardium. Intercellular dye transfer between RTEF-1 transgenic cardiac myocytes confirmed impaired conduction at the cellular level. Conduction defects were correlated with dephosphorylation of connexin40 and connexin43 and upregulation of protein phosphatase 1beta (PP1beta). Overexpression of PP1beta in HeLa cells dephosphorylated cardiac connexin. Confocal microscopy revealed increased levels of dephosphorylated connexin43 at the cardiac gap junctions in RTEF-1 mice, suggesting that defective conduction is a result of impaired gap-junction conductance rather than assembly. CONCLUSIONS: Constitutive activation of alpha1-adrenergic signaling through the RTEF-1 transcription factor results in chronic elevation of PP1beta expression and connexin dephosphorylation. This mechanism may underlie some defects in cardiac conduction.

Animals↗
PubMed1992

Analysis of dynamic atrial dimension and function during early cardiac development in the chick embryo.

Although atrial morphologic changes are well documented, the description of early atrial function is limited. We used videomicroscopic methods to define the function of the contracting atrium in stage 16 to 24 white Leghorn chick embryos. We exposed the embryo in ovo (right side up) and imaged the ventricle, then repositioned the embryo (left side up) and imaged the atrium (n greater than or equal to 8 per stage). We traced the atrial endocardial border and then measured atrial perimeter (mm) and cross-sectional area (mm2). A 20-MHz pulsed Doppler velocity meter was used to measure atrioventricular blood velocity during atrial imaging in an additional six stage 21 embryos. Data were tested by analysis of variance and regression analysis. Mean heart rate change after repositioning was -4 +/- 1%. Atrial maximum and minimum area increased linearly versus embryo stage (y = 0.10x - 1.41, r = 0.89, p less than 0.05 and y = 0.05x - 0.67, r = 0.82, p less than 0.05, respectively). Shortening fraction (percentage of reduction) of atrial perimeter and area decreased from 32.3 +/- 2.0% to 27.5 +/- 1.8% (p less than 0.05) and 56.2 +/- 3.0% to 47.7 +/- 2.0% (p less than 0.05), respectively, from stage 16 to 24. During atrial contraction, the velocity of circumferential wall shortening increased linearly with stage (y = 0.22x - 2.08, r = 0.81, p less than 0.01); however, the velocity of lengthening was similar between stages (p = 0.45). Simultaneous atrial imaging and pulsed Doppler velocity measurement showed that passive atrioventricular flow occurred late in atrial lengthening and active atrioventricular flow occurred during atrial contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1995

Glucocorticoid stimulation interacts with sympathetic innervation to affect cardiac development in oculo.

The effects of chronic glucocorticoid stimulation and sympathetic innervation on myocardium developing in the absence of hemodynamic load were tested by grafting embryonic rat hearts into the anterior eye chamber (in oculo) of adult host rats. Myocardial grafts in control rats with normal hormonal milieu were compared with grafts in rats with chronic glucocorticoid stimulation (dexamethasone 40 micrograms/d) or glucocorticoid receptor type II blockade (RU 38486, 330 micrograms/d). Unilateral superior cervical ganglionectomy of one eye chamber prevented sympathetic innervation to one graft in each host. Two indices of growth, graft size (projected area) and terminal graft weight, were obtained. Dexamethasone treatment increased both size and weight of sympathetically innervated grafts, whereas RU486 treatment significantly decreased graft weight. Conversely, dexamethasone treatment decreased graft size in denervated eye chambers, whereas RU486 treatment had no effect. No differences in graft beating rate were observed among conditions. Sympathetic innervation modulated the effect of glucocorticoids on developing myocardium, suggesting that growth of sympathetically innervated myocardium is enhanced with glucocorticoid exposure, but growth of noninnervated myocardium (e.g. fetal heart) may be compromised by excessive glucocorticoid exposure.

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