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  • 1
    Electronic Resource
    Electronic Resource
    Mast cell-mediated induction of ICAM-1, VCAM-1 and E-selectin in endothelial cells in vitro: constitutive release of inducing mediators but no effect of degranulation (1997)
    Springer
    Pflügers Archiv 435 (1997), S. 137-144 
    Details
    ISSN: 1432-2013
    Keywords: Key words Mast cells ; Endothelial cells ; Cell adhesion molecules ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Mast cell (MC)-mediated induction of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and of E-selectin was studied in cultures of rat heart endothelial cells (EC) and human umbilical vein EC (HUVEC) respectively. MC induced VCAM-1 and E-selectin, but hardly any ICAM-1 in EC. Induction was not dependent on MC degranulation, but seemed to be provoked by constitutively released substances, other than histamine, from MC. Co-incubation of MC and EC, allowing for direct contact between the two cell types, was more potent in induction than MC co-incubated separately from EC using a permeable membrane. MC were less potent in induction than exogenous added cytokines or LPS. Induction of cell adhesion molecules in rat heart EC was MC-specific, since EC incubations with either rat cardiomyocytes or heart fibroblasts had no effect. The data show that rat MC, independent of degranulation, secrete mediators relevant for the induction of a specific set of EC adhesion molecules in vitro. This suggests a (supportive) role for MC in cell-adhesion molecule induction in the endothelium in settings of early or mild inflammation. The results are discussed in the context of inflammatory processes in the heart in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050493
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  • 2
    Electronic Resource
    Electronic Resource
    Transcriptional regulation of metabolic processes: implications for cardiac metabolism (1998)
    Springer
    Pflügers Archiv 437 (1998), S. 2-14 
    Details
    ISSN: 1432-2013
    Keywords: Key words gene expression ; transcription factors ; metabolism ; hypertrophy ; heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Under normal conditions the oxidation of fatty acids and glucose covers, respectively, approximately 65% and 30% of the energy demand of the beating heart. Evidence is accumulating that various pathophysiological conditions are associated with overt changes in cardiac energy metabolism. For instance, in diabetes cardiac energy conversion relies even more on fatty acid than on glucose oxidation. In contrast, during cardiac hypertrophy the opposite takes place, i.e. the utilization of carbohydrates increases at the expense of lipids. The mechanisms responsible for and the significance of these metabolic adaptations are largely unknown. A growing body of evidence indicates that these metabolic adaptations are brought about, at least in part, through adjustments in the rate of transcription of genes encoding proteins involved in substrate transport and metabolism. There are reasons to believe that the transcriptional regulation of these ”metabolic genes” is subject to modulation by metabolites per se, i.e. by oxygen, glucose and fatty acids. In this review the concept of metabolic remodelling as an important facet of cardiac adaptation to chronic pathophysiological conditions is introduced and the putative roles of metabolites in transcriptional regulation in the heart are considered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050739
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  • 3
    Electronic Resource
    Electronic Resource
    Fatty acid-binding proteins in the heart (1998)
    Springer
    Molecular and cellular biochemistry 180 (1998), S. 43-51 
    Details
    ISSN: 1573-4919
    Keywords: myocardium ; fatty acid metabolism ; fatty acid uptake ; fatty acid-binding protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Long-chain fatty acids are important fuel molecules for the heart, their oxidation in mitochondria providing the bulk of energy required for cardiac functioning. The low solubility of fatty acids in aqueous solutions impairs their cellular transport. However, cardiac tissue contains several proteins capable of binding fatty acids non-covalently. These fatty acid-binding proteins (FABPs) are thought to facilitate both cellular uptake and intracellular transport of fatty acids. The majority of fatty acids taken up by the heart seems to pass the sarcolemma through a carrier-mediated translocation mechanism consisting of one or more membrane-associated FABPs. Intracellular transport of fatty acids towards sites of metabolic conversion is most likely accomplished by cytoplasmic FABPs. In this review, the roles of membrane-associated and cytoplasmic FABPs in cardiac fatty acid metabolism under (patho)physiological circumstances are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006878621126
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  • 4
    Electronic Resource
    Electronic Resource
    Phospholipase A2-mediated hydrolysis of cardiac phospholipids: The use of molecular and transgenic techniques (1998)
    Springer
    Molecular and cellular biochemistry 180 (1998), S. 65-73 
    Details
    ISSN: 1573-4919
    Keywords: myocardial ischemia ; ischemia-reperfusion ; phospholipid metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Under pathophysiological conditions, like myocardial ischemia and reperfusion, cardiac phospholipid homeostasis is severely disturbed, resulting in a net degradation of phospholipids and the accumulation of degradation products, such as lysophospholipids and (non-esterified) fatty acids. The derangements in phospholipid metabolism are thought to be involved in the sequence of events leading to irreversible myocardial injury. The net degradation of phospholipids as observed during myocardial ischemia may result from increased hydrolysis and/or reduced resynthesis, while during reperfusion hydrolysis is likely to prevail in this net degradation. Several studies indicate that the activation of phospholipases A2 plays an important role in the hydrolysis of phospholipids. In this review current knowledge regarding the potential role of the different types of phospholipases A2 in ischemia and reperfusion-induced damage is being evaluated. Furthermore, it is indicated how recent advances in molecular biological techniques could be helpful in determining whether disturbances in phospholipid metabolism indeed play a crucial role in the transition from reversible to irreversible myocardial ischemia and reperfusion-induced injury, the knowledge of which could be of great therapeutic relevance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006886906105
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  • 5
    Electronic Resource
    Electronic Resource
    Heat stress pretreatment mitigates postischemic arachidonic acid accumulation in rat heart (1998)
    Springer
    Molecular and cellular biochemistry 185 (1998), S. 205-211 
    Details
    ISSN: 1573-4919
    Keywords: heart ; heat stress ; ischemia ; reperfusion ; hemodynamics ; creatine kinase ; phospholipids ; arachidonic acid ; fattt acids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Heat stress pretreatment of the heart is known to protect this organ against an ischemic/reperfusion insult 24 h later. Degradation of membrane phospholipids resulting in tissue accumulation of polyunsaturated fatty acids, such as arachidonic acid, is thought to play an important role in the multifactorial process of ischemia/reperfusion-induced damage. The present study was conducted to test the hypothesis that heat stress mitigates the postischemic accumulation of arachidonic acid in myocardial tissue, as a sign of enhanced membrane phospholipid degradation. The experiments were performed on hearts isolated from rats either 24 h after total body heat treatment (42°C for 15 min) or 24 h after sham treatment (control). Hearts were made ischemic for 45 min and reperfused for another 45 min. Heat pretreatment resulted in a significant improvement of postischemic hemodynamic performance of the isolated rat hearts. The release of creatine kinase was reduced from 30 ± 14 (control group) to 17 ± 5 units/g wet wt per 45 min (heat-pretreated group) (p 〈 0.05). Moreover, the tissue content of the inducible heat stress protein HSP70 was found to be increased 3-fold 24 h after heat treatment. Preischemic tissue levels of arachidonic acid did not differ between heat-pretreated and control hearts. The postischemic ventricular content of arachidonic acid was found to be significantly reduced in heat-pretreated hearts compared to sham-treated controls (6.6 ± 3.3. vs. 17.8 ± 12.0 nmol/g wet wt). The findings suggest that mitigation of membrane phospholipid degradation is a potential mechanism of heat stress-mediated protection against the deleterious effects of ischemia and reperfusion on cardiac cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1016574720342
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  • 6
    Electronic Resource
    Electronic Resource
    Cytochrome P450, peroxisome proliferation, and cytoplasmic fatty acid-binding protein content in liver, heart and kidney of the diabetic rat (1999)
    Springer
    Molecular and cellular biochemistry 192 (1999), S. 53-61 
    Details
    ISSN: 1573-4919
    Keywords: diabetes mellitus ; cytochrome P450 4A ; fatty acid-binding protein ; peroxisome proliferation ; streptozotocin ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Diabetes mellitus generally results in an increased systemic fatty acid mobilization which can be associated with an increase in mitochondrial and peroxisomal β-oxidation of fatty acids in selected tissues. The latter is usually accompanied by a concomitant increase in the tissue content of cytoplasmic fatty acid-binding protein (FABP) which functions in the intracellular translocation of fatty acids. It was previously found that in liver clofibrate-induced proliferation of peroxisomes and increase in FABP expression each are dependent on the induction by cytochrome P4504A1 -mediated (CYP4A1) formation of dicarboxylic acids. We studied whether peroxisome proliferation and an increase of FABP contents in liver, heart and kidney of streptozotocin-induced diabetic rats are also accompanied by an increase of CYP4A1 activity, as this would indicate a possible regulatory role for dicarboxylic acids in peroxisome proliferation and FABP induction in diabetic organs other than liver. In livers of the diabetic rat, a concomitant increase was observed of the activities of CYP4A1 and the peroxisomal key enzyme fatty acyl-CoA oxidase (FACO) and of the FABP content. In the diabetic heart FACO activity and FABSP content also increased, but there was no induction of CYP4A1 activity. Conversely, in diabetic kidney there was no increase in FACO activity nor FABP content in spite of a marked induction of CYP4A1 activity. It is concluded that streptozotocin-induced diabetes leads to increased peroxisome proliferation and increased levels of FABP in both liver and heart, which only in liver is accompanied by an induction of the cytochrome P450 system. Consequently, it is not likely that dicarboxylic acids are involved in the induction of peroxisome proliferation in the heart.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006855214237
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  • 7
    Electronic Resource
    Electronic Resource
    Differential expression and localization of annexin V in cardiac myocytes during growth and hypertrophy (1998)
    Springer
    Molecular and cellular biochemistry 178 (1998), S. 229-236 
    Details
    ISSN: 1573-4919
    Keywords: annexin V ; cardiac myocyte ; growth ; hypertrophy ; heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Recently it was shown that annexin V is the most prominent member of the annexin family in the adult heart [1]. Amongst others, annexin V has been suggested to play a role in developmental processes. The aim of the present study was to explore whether in the heart annexin V content and localization change during maturational and hypertrophic growth, in order to obtain indications that annexin V is involved in cardiac growth processes. First, in the intact rat heart annexin V content and localization were studied during perinatal development. It was clearly demonstrated that annexin V content in total heart transiently increased in the first week after birth, from 0.79 ± 0.06 µg/mg protein at l day before birth to a peak value of 1.24 ± 0.08 µg/mg protein 6 days after birth, whereafter annexin V protein levels declined to a value of 0.70 ± 0.06 µg/mg protein at 84 days after birth (p 〈 0.05). Differences in annexin V content were also observed between myocytes isolated from neonatal and adult hearts [0.81 ± 0.09 and 0.17 ± 0.08 µg/mg protein, respectively (p 〈 0.05)]. Moreover, during cardiac maturational growth the subcellular localization of annexin V might change from a cytoplasmic to a more prominent sarcolemmal localization. Second, in vivo hypertrophy induced by aortic coarctation resulted in a marked degree of hypertrophy (22% increase in ventricular weight), but was not associated with a change in annexin V localization or content. The quantitative results obtained with intact hypertrophic rat hearts are supported by findings in neonatal ventricular myocytes, in which hypertrophy was induced by phenylephrine (10-5 M). In the latter model no changes in annexin V content could be observed either. In conclusion, the marked alterations in annexin V content during the maturational growth in the heart suggest a possible involvement of this protein in this process. In contrast, the absence of changes in annexin V content and localization in hypertrophied hearts compared to age matched control hearts suggests that annexin V does not play a crucial role in the maintenance of the hypertrophic phenotype of the cardiac muscle cell. This notion is supported by observations in phenylephrine-induced hypertrophied neonatal cardiomyocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006803900554
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  • 8
    Electronic Resource
    Electronic Resource
    Depletion of endogenous dopamine stores and shift in β-adrenoceptor subtypes in cardiac tissue following five weeks of chronic denervation (1998)
    Springer
    Molecular and cellular biochemistry 183 (1998), S. 215-219 
    Details
    ISSN: 1573-4919
    Keywords: heart ; denervation ; catcholamines ; β-adrenoceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Surgical ablation of extrinsic cardiac nerve fibers results in a chronically denervated state of the left ventricle of the heart. The present study was performed to elucidate the effect of a period of five weeks of chronic denervation on cardiac catecholamine levels in general and dopamine in particular. Moreover, the possible effect on cardiac β-adrenoceptor subtypes was investigated. Experiments were performed on adult dogs. In addition to adrenaline and noradrenaline the tissue levels of dopamine were found to be severely depressed. A significant shift from β1- to β2-adrenoceptor subtype was observed, while the total β-adrenoceptor density remained unaffected. The present findings indicate that catecholamine synthesis in chronically denervated hearts is impaired upstream of dopamine and that a shift in β-adrenoceptor subtype occurs already within a relatively short period of five weeks of denervation, and suggest that the lack of endogenous catecholamines influence the relative expression levels of the two subtypes of β-adrenoceptors present in cardiac tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006861112530
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  • 9
    Electronic Resource
    Electronic Resource
    Enzyme activity of rat tibialis anterior muscle differs between treatment with triamcinolone and prednisolone and nutritional deprivation (1999)
    Springer
    European journal of applied physiology 79 (1999), S. 274-279 
    Details
    ISSN: 1439-6327
    Keywords: Key words Prednisolone ; Triamcinolone ; Nutritional deprivation ; Muscle enzyme activity ; Glycogen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The maximal activity of a selection of enzymes involved in muscle carbohydrate handling, citric acid cycle and fatty acyl β-oxidation were studied after treatment with the fluorinated corticosteroid triamcinolone and compared to a similar treatment of the non-fluorinated corticosteroid prednisolone in an equipotent anti-inflammatory dose. Furthermore, because triamcinolone causes loss of body mass and muscle wasting, the effects of triamcinolone were investigated relative to a control group, with the same loss of body mass, due to nutritional deprivation. The study was performed in male Wistar rats in the following treatment groups: TR, triamcinolone treatment (0.25 mg · kg−1 · day−1 for 2 weeks), which resulted in a reduction of body mass (24%); ND, nutritional deprivation (30% of normal daily food intake for 2 weeks) resulting in a similar (24%) decrease of body mass as TR; PR, prednisolone treatment (0.31 mg · kg−1 · day−1 for 2 weeks), with a 10% increase in body mass; FF, free-fed control group, with a 12% increase in body mass in 2 weeks. Compared to FF, TR induced an increase in phosphofructokinase (PFK) activity (P 〈 0.01), glycogen synthase [GS(i + d)] activity (P 〈 0.05) and glycogen content (P 〈 0.01) in the tibialis anterior muscle. The PR and ND caused no alterations in PFK or citrate synthase (CS) activity compared to FF. Compared to PR, TR induced an increase in PFK (P 〈 0.01), CS (P 〈 0.05) and GS(i + d) activity (P 〈 0.01). Both TR and PR caused an increased muscle glycogen content, being more pronounced in TR (P 〈 0.05). Compared to ND, TR induced an increased CS (P 〈 0.05) and GS(i + d) activity (P 〈 0.01) and glycogen content (P 〈 0.01). The ND resulted in a decreased glycogen content compared to FF (P 〈 0.05). None of the treatments affected the activity of glycogen phosphorylase, β-hydroxyacyl coenzyme A dehydrogenase and lactate dehydrogenase. It was concluded that corticosteroids led to an increased muscle glycogen content; however, the changes in the enzymes of carbohydrate metabolism were corticosteroid type specific and did not relate to undernutrition, which accompanied the triamcinolone treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004210050506
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  • 10
    Electronic Resource
    Electronic Resource
    Acute and sustained effects of isometric and lengthening muscle contractions on high-energy phosphates and glycogen metabolism in rat tibialis anterior muscle (1998)
    Springer
    Journal of muscle research and cell motility 19 (1998), S. 373-380 
    Details
    ISSN: 1573-2657
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Previous studies have shown that lengthening contractions, in contrast to isometric contractions, readily result in sustained malfunctioning of the exercised muscles. The present study was performed to investigate whether an exercise period with many (240) lengthening contractions (LC) results in alterations in muscle high-energy phosphates and inosine monophosphate (IMP) content, different from muscles performing a few (60) lengthening or a few (60) or many (240) isometric contractions (IC). Moreover, we sought for a possible cause(s) of the inability to replenish muscle glycogen stores following LC. Rat tibialis anterior muscles were subjected in vivo to either 60 or 240LC or IC. Structural muscle damage occurred only after 240LC. The fact that tissue glycogen levels declined to a similar extent during LC and IC suggests that the energy demand was comparable during both types of exercise. Nevertheless, the observation that on the one hand tissue stores of adenine nucleotides showed a greater decline, and on the other hand the tissue content of IMP increased to a significantly higher level after LC than after IC, clearly indicates that muscle energy metabolism is more disturbed during LC than during IC. The high tissue levels of IMP may contribute to impaired mechanical function as previously observed in muscles subjected to LC. In contrast to 240IC, 24 hours after 240LC, tissue glycogen stores and high-energy phosphate levels were not restored to control values. The present findings indicate that depressed glycogen synthase activity and impaired activity of the mitochondrial marker enzyme cytochrome C oxidase probably contribute to a continuous disturbance of energy metabolism in the exercised muscles during the 24 hours following 240 LC.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005345603882
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