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At least 325 records · Page 18Linked to original sources
PubMed2000

A sphingosine-1-phosphate receptor regulates cell migration during vertebrate heart development.

Coordinated cell migration is essential in many fundamental biological processes including embryonic development, organogenesis, wound healing and the immune response. During organogenesis, groups of cells are directed to specific locations within the embryo. Here we show that the zebrafish miles apart (mil) mutation specifically affects the migration of the heart precursors to the midline. We found that mutant cells transplanted into a wild-type embryo migrate normally and that wild-type cells in a mutant embryo fail to migrate, suggesting that mil may be involved in generating an environment permissive for migration. We isolated mil by positional cloning and show that it encodes a member of the lysosphingolipid G-protein-coupled receptor family. We also show that sphingosine-1-phosphate is a ligand for Mil, and that it activates several downstream signalling events that are not activated by the mutant alleles. These data reveal a new role for lysosphingolipids in regulating cell migration during vertebrate development and provide the first molecular clues into the fusion of the bilateral heart primordia during organogenesis of the heart.

Alleles↗
PubMed1995

Fibroblast growth factor receptor is required for in vivo cardiac myocyte proliferation at early embryonic stages of heart development.

In birds and mammals, cardiac myocytes terminate mitotic activity in the neonatal period and regeneration of cardiac muscle does not occur after myocardial injury in adult hearts. Even embryonic myocytes, which actively proliferate in vivo, quickly lose mitotic activity when placed in cell culture. Several growth factors, including fibroblast growth factor (FGF), have been documented in embryonic hearts and some have been shown to influence myocyte terminal differentiation in culture. However, none of these growth factors have been shown to reactivate cell division in postmitotic myocytes nor have their in vivo functions been defined satisfactorily. To clarify the role of FGF signaling in heart growth, we prepared two retroviral vectors capable of suppressing (i) functions of FGF receptors (FGFRs) with a dominant-negative mutant of receptor type 1 (FGFR1) or (ii) the translation of endogenous FGFR1 by transcribing its antisense RNA. Both vectors inhibited myocyte proliferation and/or survival during the first week of chicken embryonic development but had much less effect after the second week. No apparent alteration of myocyte growth was observed after overexpression of full-length FGFR1. These results suggest that receptor-coupled FGF signaling regulates cardiac myocyte growth during tubular stages of cardiogenesis but that myocyte growth becomes FGF-independent after the second week of embryogenesis.

Animals↗
PubMed2006

Vitamin E increases the risk of developing heart failure after myocardial infarction: Results from the GISSI-Prevenzione trial.

OBJECTIVE: Although results from basic science suggested a protective role of vitamin E treatment in the prevention of cardiovascular disease, recent evidence indicates increased cardiovascular mortality due to vitamin E treatment. Recently, the HOPE trial showed an increment of the incidence of congestive heart failure (CHF) in patients treated with vitamin E. METHODS: We explored the effect of vitamin E on development of CHF in 8415 postinfarction patients without CHF at baseline, with an echocardiographic measure of left ventricular ejection fraction, who have been followed up for 3.5 years in the GISSI-Prevenzione trial. CHF during follow-up was defined as hospitalization or death for CHF. Cox regression models adjusted for relevant prognostic indicators were fitted. RESULTS: Main clinical characteristics were balanced in the 4202 and 4213 patients allocated vitamin E and control group, respectively. During follow-up, 220 patients (2.6%) developed CHF. Patients allocated vitamin E had a nonsignificant 20% (95% confidence intervals 0.92-1.56, P = 0.18) increased risk of developing CHF. Vitamin E treatment, however, was associated with a significant 50% increase (95% confidence intervals 1.03-2.20, P = 0.034) of CHF in patients with left ventricular dysfunction (ejection fraction < 50%). CONCLUSIONS: Our results confirm and extend previous evidence on the possible harmful effect of vitamin E on ventricular function in patients with cardiovascular disease. Available evidence should discourage the use of vitamin E in patients with left ventricular dysfunction.

Antioxidants↗
PubMed2001

Expression of bone morphogenetic protein-5 gene during chick heart development: possible roles in valvuloseptal endocardial cushion formation.

The bone morphogenetic protein (BMP) family, comprising multifunctional peptide growth factors, regulates many developmental processes in a variety of tissues. We examined the spatiotemporal expression of BMP5 by in situ hybridization in chick embryonic hearts from stages 5 to 33. The BMP5 gene was first expressed in the endoderm underlying the precardiac mesoderm at stages 5 to 8. Thereafter, BMP5 expression was restricted to the myocardium of the atrioventricular (AV) canal and outflow tract (OT) regions, where the valvuloseptal endocardial cushion tissue is induced. These results suggest that BMP5 may play important roles not only in myocardial differentiation, but also in the formation and maintenance of endocardial cushion tissue.

Animals↗
PubMed1990

Expression of genes encoding two chains of the collagen type VI molecule during human fetal heart development.

Northern blot analysis was used to demonstrate the expression of genes encoding two chains of the extracellular matrix molecule, collagen type VI, in human fetal heart tissue. Both genes have been mapped to the Down's obligate region of chromosome 21. As congenital heart malformations are a common feature of Down's syndrome, developmentally regulated structural protein genes encoded by chromosome 21 are being investigated.

Blotting, Northern↗
PubMed1982

Quantification of tropomyosin by radioimmunoassay in developing hearts of cardiac mutant axolotls, Ambystoma mexicanum.

Recessive mutant gene c in axolotls results in a failure of embryonic heart function. Earlier morphological studies showed that the mutant myocardial cells lack organized sarcomeric myofibrils. Electrophoresis and immunofluorescent studies suggested that the mutant heart cells contain substantial amounts of actin, myosin and alpha-actinin; however, tropomyosin appeared deficient. In the present study, we employed a newly developed extremely sensitive solid-phase radioimmunoassay method to quantitate very accurately the tropomyosin levels in normal and mutant sibling hearts at early (stage 35), intermediate (stage 39) and late (stage 41) developmental stages. Our results demonstrate that cardiac mutant hearts contain significantly lower than normal quantities of antigenically detectable tropomyosin at all of the developmental stages examined. This insufficiency of tropomyosin in mutant hearts may be a primary cause at the cell level for their failure to form organized myofibrils.

Ambystoma↗
PubMed1978

Post-weaning heart development and dietary lipid level in the male rat: evolution of lipoprotein lipase activity.

The wet weight evolution and specific and total lipoprotein lipase (LPL) activities of the heart were studied in male rats fed with diets containing 4, 12 or 21 p. 100 lipids from 50 g (3 weeks age) to 400 g body weight (13 weeks of age). The animals were compared at 100, 150, 200 and 400 g. The main results show that:--a lipid-rich diet caused some cardiac hypertrophy beginning at 100 g body weight:--specific LPL activity (activity/g of wet tissue) in the 50-400 g interval was higher when the diet contained more lipids;--when the diet contained 4 p. 100 and 12 p. 100 lipids, specific LPL activity decreased from weaning until a plateau was reached at 200 g body weight. On the other hand, when the diet contained 21 p. 100 lipids, specific LPL activity increased to a maximum in the 150-200 g interval; it then declined rapidly so that at 400 g there were no longer significant differences between the specific LPL cardiac activities of the three groups of animals. The activities thus became independant of the dietary lipid level;--total LPL cardiac activity was higher when the diet contained more lipids, at least up to the 400 g stage. When the diet contained 4 and 12 p. 100 lipids, the activity increased linearly in the 100-400 g interval. When the diet contained 21 p. 100 lipids, it increased very rapidly in the 50-200 g interval then decreased in the 200-400 g interval. In the latter interval, the differences between LPL activities of the three groups were less so that at 400 g there was only significant difference between the extreme high and low lipid groups. Thus, as specific activity, total LPL cardiac activity tended to become independent of dietary lipid level when the animals became adult.

Animals↗
PubMed1991

[Localized 31 phosphorus NMR spectroscopy of the human heart--development of a measuring method and initial clinical application].

In this work, the technique of 31P-NMR-spectroscopy is applied for the first time to diagnose coronary heart disease in patients, using a suitable measuring technique. In 13 healthy volunteers we applied a method comfortable and tolerable for patients, which enabled us to examine the myocardium inside the reception area of a surface coil. Concerning myocardium-specific selectivity and sensitivity the localization techniques FROGS (Fast-ROtating-Gradient-Spectroscopy), 1-D-ISIS (1-Dimensional-Image-Selected-In-vivo-Spectroscopy) and 3-D-ISIS were compared. By a combination of the 3-D-ISIS-technique with magnetic resonance imaging, we obtained a monitored position of the volume of interest (VOI) within the myocardium, thus gaining a selective measurement. The cube-shaped VOI with a lateral length of 50 mm was placed into the apical-septal area of the myocardium. On the basis of the obtained results, we examined seven patients suffering from coronary heart disease, which was symptomatic and verified by coronary angiography. The 31P-NMR-spectra of the two examined groups were computed into numbers representing the relative content of the myocardial high-energy-phosphates. In addition, the quotients PCr/ATP and Pi/ATP were calculated and compared. With this small number of cases the evaluation of the PCr/ATP-ratios already showed a significant difference of 0.34 (p less than 0.01) between patients with coronary heart disease (0.49 +/- 0.19) and healthy volunteers (0.83 +/- 0.27). The findings suggest the conclusion that 31P-NMR-spectroscopy is able to be instrumental in the diagnostic detection assessment of the metabolic state in coronary heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed2004

Expression of the IKr components KCNH2 (rERG) and KCNE2 (rMiRP1) during late rat heart development.

To understand molecular mechanisms that regulate formation and maintenance of cardiac IKr (rapidly activating component of the delayed rectifier K+ current), we have investigated the spatiotemporal expression pattern of two rat potassium voltage-gated channels, namely subfamily H (eag-related), member2 (KCNH2) (alias name: rERG) and Isk-related family, member2 (KCNE2) (alias name: rMiRP1) during late embryonic development by means of the in situ hybridization technique. KCNE2 is transcribed predominantly in atrial und ventricular myocardium at stages E14.5-E18.5dpc and only a minor signal emerged in the tongue at E16.5dpc. In contrast, KCNH2 transcripts appeared in a less confined pattern with intense signals in atrial and ventricular myocardium, somites, spinal cord, bowel system, central nervous system and thymus at stages E14.5-E18.5dpc. Non-cardiac expression even exceeds the intensity of the cardiac signal, indicating that KCNH2 contributes to K+ currents in non-cardiac tissue as well. Transcription of the rat b-subunit KCNE2 is present in all regions of the fetal myocardium and co-distributes perfectly with transcription of the pore forming a-subunit KCNH2. It seems likely that KCNH2 and KCNE2 are linked to form cardiac IKr channels, associated to cardiogenesis and cardiomyocyte excitability.

Animals↗