Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial ischemia reperfusion results in an increase in intracellular sodium concentration, which secondarily increases intracellular calcium via Na(+)-Ca2+ exchange, resulting in cellular injury. Endoxin is an endogenous medium of digitalis receptor and can remarkably inhibit Na+/K(+)-ATPase activity. Although the level of plasma endoxin is significantly higher during myocardial ischemia, its practical significance is unclear. This research is to investigate whether endoxin is one of important factors involved in myocardial ischemia reperfusion injury. Ischemia reperfusion injury was induced by 30 min of global ischemia and 30 min of reperfusion in isolated rat hearts. Heart rate (HR), left ventricular developed pressure (LVDP), and its first derivative (+/-dp/dtmax) were recorded. The endoxin contents, intramitochondrial Ca2+ contents, and the Na+/K(+)-ATPase activity in myocardial tissues were measured. Myocardial damages were evaluated by electron microscopy. The endoxin and intramitochondrial Ca2+ contents in myocardial tissues were remarkably higher, myocardial membrane ATPase activity was remarkably lower, the cardiac function was significantly deteriorated, and myocardial morphological damages were severe in myocardial ischemia reperfusion group vs. control. Anti-digoxin antiserum (10, 30 mg/kg) caused a significant improvement in cardiac function (LVDP and +/-dp/dtmax), Na+/K(+)-ATPase activity, and myocardial morphology, and caused a reduction of endoxin and intramitochondrial Ca2+ contents in myocardial tissues. In the present study, the endoxin antagonist, anti-digoxin antiserum, protected the myocardium against the damages induced by ischemia reperfusion in isolated rat hearts. The results suggest that endoxin might be one of main factors mediating myocardial ischemia reperfusion injury.
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PMID:Endoxin-mediated myocardial ischemia reperfusion injury in rats in vitro. 1538 64

Epidemiological data document that regular exercise protects against the morbidity and mortality associated with ischemic heart disease. Therefore, we tested the hypothesis that daily exercise (DE) increases the ventricular arrhythmia threshold (VAT) induced by coronary artery occlusion and alters the expression of calcium regulatory proteins. The VAT was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. To test this hypothesis, we recorded the VAT in conscious sedentary normotensive, sedentary hypertensive, and DE hypertensive rats, and we associated these thresholds with the protein expression of the L-type calcium channel, Na+/Ca2+ exchanger, phospholamban, and sarco(endo)plasmic reticulum Ca(2+)-ATPase. Results document a significantly reduced time to ventricular arrhythmias (sedentary hypertensive, 3.7 +/- 0.3 min vs. sedentary normotensive, 4.8 +/- 0.3 min), an increased Na+/Ca2+ exchanger protein expression (47%), and a decreased phospholamban protein expression (-34%) in conscious hypertensive rats. DE increased the VAT (5.9 +/- 0.2 min), decreased the protein expression of the Na+/Ca2+ exchanger, and normalized the protein expression of phospholamban in the hypertensive rats. Thus DE may be a primary prevention approach for reducing the incidence of arrhythmias by altering calcium regulatory proteins in hypertensive rats.
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PMID:Daily exercise-induced cardioprotection is associated with changes in calcium regulatory proteins in hypertensive rats. 1547 72

N-n-butyl haloperidol iodide (F2), a novel compound derived from haloperidol, was synthesized by our drugs research lab. The present study aims to evaluate the protective effects of F2 on myocardial ischemia-reperfusion injury in vivo, and to try to find the protective mechanism of F2. The animal model of myocardial ischemia-reperfusion injury was established by ligaturing rabbit's left ventricular branch of coronary artery for 40 min and removing the ligation later to reperfuse for 40 min. Different doses of F2 were intravenously injected before the onset of ischemia. The changes of hemodynamics were recorded during the experiment, and the activities of superoxide dismutase (SOD), creatine kinase (CK), Ca2+-ATPase, Na+,K+-ATPase and the level of malondialdehyde (MDA) of myocardial tissue were detected after reperfusion. Administration of F2 could dose-dependently ameliorate the hemodynamics of ischemia-reperfusion injured myocardium. During the course of reperfusion, MAP, LVSP, +/-dP/dt(max) in all F2 groups were obviously higher than those in the ischemia-reperfusion control group, and LVEDP were lower. F2 could also reduce the production of MDA, and maintain the activities of SOD, Ca2+-ATPase, Na+,K+-ATPase, and minimize the leakage of CK out of myocardial cells in a dose-dependent manner. These results suggested that F2 had apparent protective effects against myocardial ischemia-reperfusion injury.
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PMID:Protective effects of N-n-butyl haloperidol iodide on myocardial ischemia-reperfusion injury in rabbits. 1548 87

This article includes historical sketch of magnesium research, basic researches on effect of magnesium on cardiovascular disease, practical researches (including clinical studies) on relationship between magnesium intake and cardiovascular disease and current status of intake amount of magnesium in Japanese estimated by the national nutrition survey in Japan, 2002. Basic studies revealed the mechanism that magnesium deficiency may decrease ATPase, leading to increase in intracellular calcium of blood vessels, and then the vasoconstriction occurs in cardiovascular system. Clinical studies clarified that magnesium levels in serum decreased significantly in patients with ischemic heart disease. The National Nutrition Survey in Japan revealed that intake amount of magnesium of people for 15 - 49 year male and female were below the recommended dietary allowance of magnesium in Japan.
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PMID:[Magnesium intake and cardiovascular disease]. 1569 52

Physiological stresses (heat, hemodynamics, genetic mutations, oxidative injury and myocardial ischemia) produce pathological states in which protein damage and misfolded protein structures are a common denominator. The specialized proteins family of antistress proteins - molecular chaperons (HSPs) - are responsible for correct protein folding, dissociating protein aggregates and transport of newly synthesized polypeptides to the target organelles for final packaging, degradation or repair. They are inducible at different cell processes such as cell division, apoptosis, signal transduction, cell differentiation and hormonal stimulation. HSPs are involved in numerous diseases including cardiovascular pathologies, revealing changes of expression and cell localization. We studied the possible changes in expression level of abundant mitochondrial chaperon Hsp60 and main human cytochrome P450 monooxygenase (2E1 isoform) at dilated cardiomyopathy (DCM) progression at the end stage of heart failure using Western blot analysis. The ischemic and normal humans' hearts were studied as control samples. We observed the decrease of Hsp60 level in cytoplasmic fraction of DCM- and ischemia-affected hearts' left ventricular and significant increase of Hsp60 in mitochondrial fractions of all hearts investigated. At the same time we detected the increase of P450 2E1 expression level in ischemic and dilated hearts' cytoplasmic fractions in comparison with normal myocardium and no detectable changes in microsomal fractions of hearts investigated which could be linked with increased level of oxidative injury for DCM heart muscle. In addition, all the changes described are accompanied by significant decrease of ATPase activity of myosin purified from DCM-affected heart in comparison with normal and ischemic myocardia as well. The data obtained allow us to propose a working hypothesis of functional link between antistress (HSPs) and antioxidative (cytochromes) systems at DCM progression.
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PMID:Molecular chaperone, HSP60, and cytochrome P450 2E1 co-expression in dilated cardiomyopathy. 1576 99

Pathological circumstances like inflammation or ischemic insult facilitate the release of adenine nucleotides from several types of cells. These extracellular nucleotides are rapidly converted to adenosine by ectonucleotidases, mainly ectonucleoside triphosphate diphosphohydrolase1 (NTPDase1/CD39) and CD73. NTPDase1/CD39 can interact with caveolins, structural proteins of signal-transducing microdomains termed caveolae. Caveolins are thought to have physiological roles in heart ageing and cardiac diseases. The aim of this study was to investigate the expression of NTPDase1 together with caveolins in chronic human cardiovascular diseases and elucidate their role in human heart. The HPLC analysis showed significant increase in ATPase activity in pathological samples from patients with ischemic heart disease. Immunostaining also showed alterations in the expression and distribution of NTPDase1. Caveolin-1 and caveolin-2 expression was much alike in control and pathological cases, while expression of caveolin-3 was lower in pathological samples. Changes in the expression of NTPDase1 and caveolins seem to be independent of human cardiovascular disease.
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PMID:Expression of NTPDase1 and caveolins in human cardiovascular disease. 1602 70

Drug-induced delayed cardiac protection (DCP) against the effects of acute myocardial ischemia was first described 22 years ago by the author and his coworkers. It can be initiated by noninjurious pharmacological doses of prostacyclin (PGI2), its stable analogues, and by catecholamines. DCP protects against many consequences of ischemia, attenuating early morphological changes, limiting infarct size and suppressing arrhythmias, and can also protect against ouabain intoxication. DCP operates under a variety of pathological conditions (atherosclerosis, hypercholesterolaemia, and diabetes). DCP can also be evoked by transient myocardial ischemia and by exercise and is known in this context as "ischemic preconditioning", specifically the "second window of protection"; transient ischemia also evokes an immediate but short-lived protection known as "classical preconditioning". DCP is fundamentally different in concept to conventional drug therapy because the process appears to depend on the duration of the trigger and be related in a bell-shaped manner to the strength of the trigger. The exact mechanism is uncertain. Prolongation of the effective refractory period (ERP) and of the action potential duration (APD) may contribute to DCP suppression of arrhythmias. The protection is time and dose dependent, with optimal effects 24 to 48 hr after treatment. It can be sustained by intermittent administration of low maintenance doses. Stimulation of the adenylate-cyclase/cyclic adenosine monophosphate (cAMP) system appears to be a common feature of DCP. Responses to beta-adrenergic stimuli are also diminished. Cardiac cAMP triggers the induction of phosphodiesterase (PDE) 1 and 4 isoforms and of Na/K-ATPase. Increased amount and activity of PDE isoforms subsequently reduces excess myocardial cAMP production. Changes in Na/K-ATPase moderate ischemic myocardial potassium loss, sodium, and calcium accumulation, as well as the toxicity of ouabain. The future therapeutic challenge is to identify new drugs that can mimic DCP.
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PMID:Drug-induced delayed cardiac protection against the effects of myocardial ischemia. 1609 98

Hyperlipidemia is a major risk factor for the premature development of coronary heart disease and it has been shown to increase the incidence of myocardial ischemia and cardiac events. Pentacyclic triterpenes possess antiatherosclerotic, antioxidant, anti-inflammatory and cytoprotective effects. To study the effect of plant derived triterpene, lupeol and its ester lupeol linoleate, on lipid status and biochemical changes on heart tissue, male albino Wistar rats were fed high-cholesterol diet (normal rat chow supplemented with 4% cholesterol and 1% cholic acid; HCD) for 30 days. There was a significant (p<0.001) increase in the levels of total cholesterol, triglycerides and phospholipids along with augmented activities of lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase in the heart tissue. Triterpenes treatment reduced the above alterations produced in hypercholesterolemic rats. The transmembrane enzymes, namely Na(+), K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase showed a decrease in their activities. Triterpenes treatment reversed these levels, prevented the hypertrophic cardiac histology and restored the normal ultrastructural architecture. In conclusion, lupeol and lupeol linoleate intervention minimized the lipid abnormalities and abnormal biochemical changes induced by HCD fed rats. This shows that triterpenes possess cardioprotective effects which will be beneficial in hypercholesterolemic condition. Out of these two triterpenes tested, lupeol linoleate appeared to be even more effective than lupeol.
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PMID:Protective effect of lupeol and its ester on cardiac abnormalities in experimental hypercholesterolemia. 1733 64

This study was designed to investigate the protective effect of oleanolic acid (OA) against isoproterenol-induced myocardial ischemia in rat myocardium. Wistar strain rats were pretreated with OA (20, 40, and 60 mg/kg, s.c) for 7 days and then intoxicated with isoproterenol (ISO, 85 mg/kg, sc for 2 consecutive days). Heart were excised from the experimental animals and assessed for the activities of marker enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)], the levels of lipid peroxide products [thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (HP) and conjugated dienes (CD)], myeloperoxidase (MPO), lipid profiles [total cholesterol (TC), free cholesterol, ester cholesterol, triglycerides (TG), free fatty acids (FFA) and phospholipids (PL)], and membrane-bound ATPase enzymes (total ATPase, Na(+)K(+) ATPase, Ca(2 +) ATPase, and Mg(2 +) ATPase). Troponin T and I were estimated in plasma. Leakage of cardiac markers, elevated lipid peroxidation with increased lipid profiles and decreased activities of membrane-bound ATPase enzymes were confirmed the severe myocardial damage occurring as a consequence of isoproterenol-induced ischemia, and they also showed the significant improvement effected by oleanolic acid pretreatment. These findings provided evidence that oleanolic acid was found to be protecting rat myocardium against ischemic insult and the protective effect could attribute to its anti-oxidative, anti-hyperlipedemic, and anti-arrhythmic properties as well as its membrane-stabilizing action.
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PMID:Cardioprotective effect of oleanolic acid on isoproterenol-induced myocardial ischemia in rats. 1745 91

Sarcolipin (SLN) is a small molecular weight sarcoplasmic reticulum (SR) membrane protein expressed both in cardiac and skeletal muscle tissues. Recent studies using transgenic mouse models have demonstrated that SLN is an important regulator of cardiac SR Ca2+ ATPase 2a (SERCA2a). However, there is a paucity of information regarding the SLN protein expression in small versus larger mammals and its regulation during development and cardiac pathophysiology. Therefore, the major goal of this study was to generate an SLN specific antibody and perform detailed analyses of SLN protein expression during muscle development and in the diseased myocardium. The important findings of the present study are: (i) in small mammals, SLN expression is predominant in the atria but low in the ventricle and in skeletal muscle tissues, whereas in large mammals, SLN is quite abundant in skeletal muscle tissues than the atria, (ii) SLN and SERCA2a are co-expressed in all striated muscle tissues studied except ventricle and co-ordinately regulated during muscle development and (iii) SLN protein levels are approximately 3 fold upregulated in the atria of heart failure dogs and approximately 30% decreased in the atria of hearts prone to myocardial ischemia. In addition we found that in the phospholamban null atria, SLN protein levels are upregulated.
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PMID:Differential expression of sarcolipin protein during muscle development and cardiac pathophysiology. 1756 Nov 7


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