Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The alteration of sarcolemmal membrane permeability of cardiac muscle cells in rats fed grain from a Keshan disease (KD) endemic area was studied with horseradish peroxidase (HRP) as a tracer. Weanling male rats were divided at random into three groups and fed the following three diets, respectively, for 3 months: a diet with grain from a KD endemic area (Group A), a diet with grain from a KD nonendemic area (Group B), and standard laboratory chow (Group C). At the end of the experiment, HRP was injected intravenously and localized in the ventricular myocardium by light microscopy. The experimental results showed that the percentage of cardiac muscle cells containing HRP reaction product in rats fed grain from the KD endemic area was significantly greater than that in rats fed grain from nonendemic area and standard laboratory chow. This suggests that the sarcolemmal membrane permeability of cardiac muscle cells in rats of Group A was markedly increased. The distribution of cardiac muscle cells with increased sarcolemmal membrane permeability was similar to that seen in the myocardium of KD patients. The present study suggests that the abnormal membrane permeability of cardiac muscle cells may play an important role in the pathogenesis of myocardial necrosis in KD.
Exp Mol Pathol 1989 Jun
PMID:Increased sarcolemmal membrane permeability of cardiac muscle cells in rats fed grains cultivated in a Keshan disease endemic area: a study with horseradish peroxidase as a tracer. 272 51

A new protein was found at the site of interaction of cytoskeletal filaments and the plasma membrane in desmosomes of human cardiac muscle intercalated discs. As revealed by the indirect immunofluorescence method, monoclonal antibody XVE2 was able to stain intercalated discs of cardiac muscle and desmosomes of human skin epidermal cells, whereas it did not react with sections from human uterine smooth muscle, vascular tissue and liver. Western immunoblot analysis of extracts of total human heart and uterus demonstrated that a doublet of 65 kDa and 70 kDa polypeptides were the major proteins recognized by the monoclonal antibody XVE2. These 65 kDa and 70 kDa proteins are immunologically distinct from other known intercalated disc proteins such as vinculin, meta-vinculin, filamin, talin, alpha-actinin, desmin and desmoplakins. The distribution of the XVE2 monoclonal antibody antigens raises the possibility that these polypeptides are involved in linking intermediate filaments to the dense plaque of desmosomes of cardiac muscle intercalated discs.
J Mol Cell Cardiol 1989 Feb
PMID:Identification and immunolocalization of a new component of human cardiac muscle intercalated disc. 273 27

Energy metabolism of quiescent cardiac muscle was studied in the isolated rabbit heart preparation perfused at constant pressure by the Langendorff technique. Oxygen consumption (MVo2), coronary flow rate (CFR) and the steady state concentrations of high energy phosphate compounds were determined in hearts rendered asystolic using modified Krebs-Henseleit (KH) media containing 11 mM glucose as substrate. Basal MVo2 and CFR were significantly higher in hearts arrested by Ca2+ depletion (low Ca KH) compared to K+ excess (high K KH). Substitution of glucose in low Ca KH with a mixture containing glutamate, fumarate and pyruvate (low Ca KH + GFP) resulted in a 25% increase in the basal MVo2 but a 20% decline in CFR. Supplementing the low Ca perfusate with 30 g/l dextran (low Ca KH + dextran) depressed both the basal MVo2 (35%) and CFR (75%). Differences in the basal MVO2 under the different perfusion conditions were not accompanied by significant changes in the tissue levels of ATP, CrP or Cr. Compared to low Ca KH arrested hearts, those perfused with low Ca KH + GFP or low Ca KH + dextran did, however, show significantly lower tissue levels of ADP, AMP and Pi, but higher cytosolic ratios of [ATP]/[ADP][Pi] and [CrP]/[Cr][Pi]. As a consequence of the higher phosphorylation potential the free energy of ATP hydrolysis increased. There was no significant difference in any of these parameters between high K KH and low Ca KH perfused hearts. It is concluded that in the perfused, arrested heart none of the parameters that are used to describe the myocardial energetic state, e.g. free [ADP] or the cytosolic [ATP]/[ADP][Pi] ratio, uniquely correlates with the basal metabolic rate as estimated from MVO2 measurements.
J Mol Cell Cardiol 1989 Feb
PMID:Energy metabolism in the perfused, arrested rabbit heart. 274 50

Evidence implicating reactive oxygen species (ROS) in reperfusion-induced arrhythmias is accumulating rapidly [1,2]. However, surprisingly little is known about the effects of ROS on cardiac electrophysiology. Such knowledge would improve our understanding of reperfusion-induced arrhythmias. Photosensitizers and light are known to produce a variety of ROS. They might, therefore, be useful for investigating oxygen-mediated cell injury. To our knowledge, such an approach has not been used to investigate ROS-induced alterations in the electrophysiological properties of cardiac muscle. The purpose of this paper is to demonstrate (1) the feasibility of using photosensitizers for such an investigation, and (2) some advantages photosensitizers offer when combined with single cell and patch pipette methodologies. A comparison of the electrophysiological alterations produced by photosensitizer-generated ROS to the reported effects of xanthine-xanthine oxidase or organic hydroperoxides suggests that the electrophysiological alterations produced by superoxide initiated reactions and/or lipid peroxidation are similar to those produced by photosensitizers and light.
J Mol Cell Cardiol 1989 Jun
PMID:Modification of cardiac action potential by photosensitizer-generated reactive oxygen. 277 6

The fluorescent Ca2+ indicator fura-2 was used to follow cytosolic Ca2+ transients during excitation-contraction coupling in suspensions of isolated rat heart cells induced to beat synchronously by electrical field stimulation. The Ca2+ transient reached a maximum at about 30 ms after application of the electrical stimulus and then relaxed to the basal level over the following 200 ms. Treatment of the myocytes with 0.25 to 2.0% ethanol (40 to 340 mM) caused a decrease in the peak of the Ca2+ transient, with no apparent change in the time to peak. This effect of ethanol occurred progressively over a period of about 1 min before a new stable state was achieved. At 1% ethanol the peak Ca2+ level was reduced by 50%. Ethanol reversed the stimulatory effect of isoproterenol on peak Ca2+ and at high levels of ethanol the beta-adrenergic agonist no longer caused any enhancement of the Ca2+ transient. Ethanol did not cause any marked change in the basal Ca2+ level between beats. The effects of ethanol were readily reversible. These results suggest that the negative inotropic effect of ethanol observed in intact cardiac muscle preparations may result in part from interference with the Ca2+ fluxes responsible for excitation-contraction coupling in ventricular myocytes.
J Mol Cell Cardiol 1989 Jun
PMID:Ethanol inhibits electrically-induced calcium transients in isolated rat cardiac myocytes. 277 7

The metabolism of pantothenic acid (Pa) by cardiac muscle was studied in normal and diabetic rats. Tissue levels of Coenzyme A (CoA) are elevated in the heart during early (6 to 12 h) diabetes, remains at a high level for several days, and then returns to normal or below normal levels. The increase in total tissue CoA mainly occurs in myocytes as indicated by isolation of cardiac myocytes from control and diabetic animals and measuring their content of CoA. The CoA concentration increased from 37 to 93 microM in the cytosolic compartment and from 2.0 to 2.6 mM in the mitochondrial matrix. These effects of diabetes were reversed by insulin treatment. CoA synthesis in hearts removed from control rats and perfused in vitro was stimulated by including in the perfusate Pa, cysteine and dithiothreitol, but no exogenous energy substrate. This stimulated in vitro rate of CoA synthesis was reduced in hearts removed from diabetic animals, and the reduction increased with duration of diabetes. The reduced rate in diabetic hearts resulted from both a decreased rate of Pa phosphorylation and decreased Pa transport. Transport of Pa into myocytes was decreased by as much as 80% in hearts from diabetic animals. The low transport rate was due to a decrease in Vmax with no apparent change in Km. Treatment of the isolated heart with insulin did not correct the diabetic-induced reduction in Pa transport. The transport rate in normal and diabetic hearts was not influenced by the type of energy substrate provided to the heart.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mol Cell Cardiol 1989 Jul
PMID:Metabolism of pantothenic acid in hearts of diabetic rats. 279 60

Muscle creatine kinase (MCK) is expressed at high levels only in skeletal and cardiac muscle tissues. Previous in vitro transfection studies of skeletal muscle myoblasts and fibroblasts had identified two MCK enhancer elements and one proximal promoter element, each of which exhibited expression only in differentiated skeletal muscle. In this study, we have identified several regions of the mouse MCK gene that are responsible for tissue-specific expression in transgenic mice. A fusion gene containing 3,300 nucleotides of MCK 5' sequence exhibited chloramphenicol acetyltransferase activity levels that were more than 10(4)-fold higher in skeletal muscle than in other, nonmuscle tissues such as kidney, liver, and spleen. Expression in cardiac muscle was also greater than in these nonmuscle tissues by 2 to 3 orders of magnitude. Progressive 5' deletions from nucleotide -3300 resulted in reduced expression of the transgene, and one of these resulted in a preferential decrease in expression in cardiac tissue relative to that in skeletal muscle. Of the two enhancer sequences analyzed, only one directed high-level expression in both skeletal and cardiac muscle. The other enhancer activated expression only in skeletal muscle. These data reveal a complex set of cis-acting sequences that have differential effects on MCK expression in skeletal and cardiac muscle.
Mol Cell Biol 1989 Aug
PMID:Muscle creatine kinase sequence elements regulating skeletal and cardiac muscle expression in transgenic mice. 279 90

Rapid mixing-vesicle ion flux and planar lipid bilayer-single channel measurements have shown that a high-conductance, ligand-gated Ca2+ release channel is present in 'heavy', junctional-derived membrane fractions of skeletal and cardiac muscle sarcoplasmic reticulum. Using the release channel-specific probe, ryanodine, a 30S protein complex composed of polypeptides of Mr approximately 400,000 has been isolated from cardiac and skeletal muscle. Reconstitution of the complex into planar lipid bilayers has revealed a Ca2+ conductance with properties characteristic of the native Ca2+ release channel.
Mol Cell Biochem
PMID:Biochemical characterization of the Ca2+ release channel of skeletal and cardiac sarcoplasmic reticulum. 284 14

Three to six mg of the millimolar Ca2+-requiring proteinase (m-calpain) were obtained from 1 kg bovine cardiac muscle (fresh wt) and some enzymatic properties of this proteinase were determined. Activity of bovine cardiac m-calpain decreases as ionic strength increases from 75 to 1000 mM. Maximal activation of m-calpain by Ca2+, La3+, Ba2+, and Mn2+ occurs at 2 to 3 mM concentrations of each of these divalent cations, but La3+ activation is only 20 to 25% and Ba2+ and Mn2+ activation only 6 to 10% as great as Ca2+ activation. Maximum Sr2+ activation occurs at 20 mM Sr2+ and is 90 to 95% of maximum Ca2+ activation. Mg2+, Zn2+, Cr2+, and Cd2+ do not activate m-calpain when added alone; Mg2+ does not affect, but Zn2+ inhibits, Ca2+-stimulated activity. The nonionic detergents, Triton X-100 and Brij 35, activate m-calpain 1.6- to 2.0-fold but do not change its Ca2+ requirement. Sodium dodecyl sulfate and urea inhibit m-calpain completely at 0.045% and 2.0 M, respectively. Because they bind Ca2+ needed for activation, ATP, ADP, and ITP inhibit m-calpain. The trypsin inhibitors, phenylmethylsulfonyl fluoride, ovomucoid trypsin inhibitor, ovoinhibitor, aprotinin, alpha 1-antiproteinase inhibitor, soybean trypsin inhibitor, and lima bean trypsin inhibitor do not affect m-calpain activity; m-calpain does not release measureable quantities of acid-soluble peptides from a rabbit skeletal sarcoplasmic protein fraction but does degrade rabbit skeletal myofibrils and casein.
J Mol Cell Cardiol 1988 Nov
PMID:Some properties of the millimolar Ca2+-dependent proteinase from bovine cardiac muscle. 285 32

The metabolic and circulatory consequences of activation of the muscarinic receptor(s) were investigated by local administration of acetylcholine and its three analogues (bethanechol, carbachol and methacholine) into beating and KCl-arrested perfused rat hearts. Acetylcholine and the three other choline esters caused vasoconstriction in both types of preparations and this vasoconstriction was accompanied by a decrease in oxygen consumption. In most cases the dose-response curves were biphasic and changes in coronary flow paralleled those in oxygen consumption. Both phenomena were abolished by administration of atropine and either removal of calcium or infusion of verapamil but were unaffected by addition of the adrenergic alpha-blocker, prazosin, and the adrenergic beta-blocker, propranolol. Infusions of low concentrations of the cholinergic agonists were accompanied by increases in the myocardial phosphorylation state ratio [( ATP]free/[ADP]free[Pi]) which correlated with the simultaneous decreases in oxygen consumption and coronary flow. It is suggested that muscarinic receptors responsible for vasoconstriction in perfused rat heart are located not only on coronary vessels but also on the cardiac muscle cells. Activation of the former receptors induces vasoconstriction by direct action on the vascular smooth muscle while activation of the latter receptors induces vasoconstriction indirectly by decreasing cardiac work and increasing the myocardial [ATP]free/[ADP]free[Pi] ratio. The results also show that stimulation of muscarinic receptor(s) and the consequent metabolic and vasoregulatory responses are coupled to calcium movements.
J Mol Cell Cardiol 1985 Jan
PMID:The effect of cholinergic agonists on coronary flow rate and oxygen consumption in isolated perfused rat heart. 285 76


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