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Chronic phospholamban-sarcoplasmic reticulum calcium atpase interaction is the critical calcium cycling defect in dilated cardiomyopathy

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CELL 1999年第3期99卷 313-322页

作者： Minamisawa, S Hoshijima, M Chu, GX Ward, CA Frank, K Gu, YS Martone, ME Wang, YB Ross, J Kranias, EG Giles, WR Chien, KR Univ Calif San Diego UCSD Salk Program Mol Med La Jolla CA 92093 USA Univ Calif San Diego Dept Med La Jolla CA 92093 USA Univ Calif San Diego Ctr Mol Genet La Jolla CA 92093 USA Univ Calif San Diego Dept Neurosci La Jolla CA 92093 USA Univ Cincinnati Coll Med Dept Pharmacol & Cell Biophys Cincinnati OH 45267 USA Univ Calgary Sch Med Dept Physiol & Biophys Calgary AB T2N 4N1 Canada

Dilated cardiomyopathy and end-stage heart failure result in multiple defects in cardiac excitation-contraction coupling. Via complementation of a genetically based mouse model of dilated cardiomyopathy, we now provide evidence that progressive chamber dilation and heart failure are dependent on a Ca2+ cycling defect in the cardiac sarcoplasmic reticulum. The ablation of a muscle-specific sarcoplasmic reticulum Ca2+ atpase (SERCA2a) inhibitor, phospholamban, rescued the spectrum of phenotypes that resemble human heart failure. Inhibition of phospholamban-SERCA2a interaction via in vivo expression of a phospholamban point mutant dominantly activated the contractility of ventricular muscle cells. Thus, interfering with phospholamban-SERCA2a interaction may provide a novel therapeutic approach for preventing the progression of dilated cardiomyopathy.

关键词：钙/代谢钙结合蛋白质类/缺乏钙结合蛋白质类/遗传学钙结合蛋白质类/代谢钙转运atp酶类/拮抗剂和抑制剂钙转运atp酶类/代谢心肌病扩张型/遗传学心肌病扩张型/病理学心肌病扩张型/病理生理学疾病模型动物疾病恶化心脏/生理学心脏/病理生理学内环境稳定小鼠基因敲除心肌收缩心肌/病理学肌浆网/酶学心室功能左动物人类小鼠

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LONG-RANGE INTRAMOLECULAR LINKED FUNCTIONS IN ACTIVATION AND INHIBITION OF SERCA atpASES

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ANNALS OF THE NEW YORK ACADEMY OF SCIENCES 1992年第1期671卷 32-48页

作者： INESI, G CANTILINA, T YU, X NIKIC, D SAGARA, Y KIRTLEY, ME Department of Biological Chemistry School of Medicine University of Maryland Baltimore Maryland 21201

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Fast calcium removal during single twitches in amphibian skeletal muscle fibres

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JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY 1999年第5-6期20卷 555-567页

作者： Caputo, C Bolaños, P Escobar, AL Inst Venezolano Invest Cient Ctr Biofis & Bioquim Lab Biofis Musculo Caracas Venezuela

Fluorescence signals from the calcium sensitive dyes Fluo-3 or Rhod-2 were obtained simultaneously with isometric tension in single fibres isolated from the anterior tibialis muscle of Leptodactylus insularis (20-22 degrees C). Fluo-3 fluorescence signals were transformed into [Ca2+](i) transients as previously described. Most of the decay phase of single twitch transient is well fitted by a single exponential (tau of about 10 ms), followed by a slower declining component lasting tens of milliseconds. During short periods, 10 to 20 s, of low frequency stimulation, between 0.2 and 5 Hz, the basal [Ca2+](i) increased slowly from 0.1 to about 0.4 mu M, with only minor changes in the exponentially decaying phase. In fibres poisoned with thapsigargin or cyclopiazonic acid (1-2 mu M) the tau of decay of fluorescence or Ca2+ transients of single twitches was very similar to that observed in non-poisoned fibres. Nevertheless, in poisoned fibres challenged with repetitive stimulation, the tau of Ca2+ transients decay increased from about 10 ms to > 40 ms, while the basal [Ca2+](i) increased from 0.1 to 2 mu M. Short rest periods (about 5 min) could reverse these effects, indicating that they were not a direct consequence of SR Ca2+-atpase inhibition. The correlation coefficient between tau of decay and basal [Ca2+](i) was > 0.8 (P < 0.0001). Qualitatively similar results were obtained measuring Rhod-2 fluorescence signals. A lumped, two-compartment model could account for these results. Loading the fibres with EGTA-AM, diminished the effects of prolonged stimulation observed in poisoned fibres. Moreover, we show that the Na+ - Ca2+ exchange mechanism does not participate appreciably in fast Ca2+ removal.

关键词：动作电位/药物作用动作电位/生理学苯胺化合物无尾目结合部位/生理学缓冲剂钙/代谢钙转运atp酶类/拮抗剂和抑制剂钙转运atp酶类/代谢电刺激电生理学酶抑制剂/药理学荧光染料等长收缩/生理学动力学镁/代谢显微镜检查荧光模型生物学肌纤维/酶学肌骨骼/细胞学肌骨骼/生理学小白蛋白/生理学反应时间/生理学钠/代谢钠钙交换蛋白/代谢毒胡萝卜内酯/药理学呫吨类动物

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Agonist-evoked mitochondrial Ca²⁺ signals in mouse pancreatic acinar cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第49期275卷 38680-38686页

作者： González, A Schulz, I Schmid, A Univ Saarland Dept Physiol D-66421 Homburg Germany

In the present study we have investigated cytosolic and mitochondrial Ca2+ signals in isolated mouse pancreatic acinar cells double-loaded with the fluorescent probes fluo-3 and rhod-2. Stimulation of pancreatic acinar cells with 500 nM acetylcholine caused release of Ca2+ from intracellular stores and produced cytosolic Ca2+ signals in form of Ca2+ waves propagating from the luminal to the basal cell pole. The increase in the cytosolic Ca2+ concentration was followed by Ca2+ uptake into mitochondria. Between onset of cytosolic and mitochondriaI Ca2+ signals there was a delay of 10.7 +/- 0.4 s. Ca2+ uptake into mitochondria could be inhibited with Ruthenium Red and carbonyl cyanide m-chlorophenylhydrazone, whereas 2,5-di-tert-butylhydroquinone, which inhibits sarco(endo)plasmic reticulum Ca2+ atpases, did not prevent Ca2+ accumulation in mitochondria. Carbonyl cyanide m-chlorophenylhydrazone-induced Ca2+ release from mitochondria could only be observed after a preceding stimulation of the cell with a physiological agonist or by treatment with 2,5 di-tertbutylhydroquinone, indicating that under resting conditions mitochondria do not contain releasable Ca2+ ions. Analysis of the propagation rate of acetylcholine-induced Ca2+ waves revealed that inhibition of mitochondrial Ca2+ uptake did not accelerate spreading of cytosolic Ca2+ signals. Our experiments indicate that in the early phase of secretagogue-induced Ca2+ signals, mitochondria behave as passive Ca2+-buffering elements and do not actively suppress spreading of Ca2+ signals in pancreatic acinar cells.

关键词：乙酰胆碱/药理学钙/代谢钙信号/药物作用钙信号/生理学钙转运atp酶类/拮抗剂和抑制剂碳酰氰化物间-氯苯基腙/药理学胞质溶胶/代谢酶抑制剂/药理学氢醌类/药理学动力学显微镜检查共焦线粒体/药物作用线粒体/生理学胰腺/细胞学胰腺/生理学钌红/药理学动物男(雄)性小鼠

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The role of luminal Ca²⁺ in the generation of Ca²⁺ waves in rat ventricular myocytes

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第1期518卷 173-186页

作者： Lukyanenko, V Subramanian, S Györke, I Wiesner, TF Györke, S Texas Tech Univ Hlth Sci Ctr Dept Physiol Lubbock TX 79430 USA Texas Tech Univ Dept Chem Engn Lubbock TX 79409 USA

1. We used confocal Ca2+ imaging and fluo-3 to investigate the transition of localized Ca2+ releases induced by focal caffeine stimulation into propagating Ca2+ waves in isolated rat ventricular myocytes. 2. Self-sustaining Ca2+ waves could be initiated when the cellular Ca2+ load was increased by elevating the extracellular [Ca2+] ([Ca2+](o)) and they could also be initiated at normal Ca2+ loads when the sensitivity of the release sites to cytosolic Ca2+ was enhanced by low doses of caffeine. When we prevented the accumulation of extra Ca2+ in the luminal compartment of the: sarcoplasmic reticulum (SR) with thapsigargin, focal caffeine pulses failed to trigger self-sustaining Ca2+ waves on elevation of [Ca2+](o). Inhibition of SR Ca2+ uptake by thapsigargin in cells already preloaded with Ca2+ above normal levels did not prevent local Ca2+ elevations from triggering propagating waves. Moreover, wave velocity increased by 20%. Tetracaine (0.75 mM) caused transient complete inhibition of both local and propagating Ca2+ signals, followed by full recovery of the responses due to increased SR Ca2+ accumulation. 3. Computer simulations using a numerical model with spatially distinct Ca2+ release sites suggested that increased amounts of releasable Ca2+ might not be sufficient to generate self-sustaining Ca2+ waves under conditions of Ca2+ overload unless the threshold of release site Ca2+ activation was set at relatively low levels (< 1.5 mu M). 4. We conclude that the potentiation of SR Ca2+ release channels by luminal Ca2+ is an important factor in Ca2+ wave generation. Wave propagation does not require the translocation of Ca2+ from the spreading wave front into the SR. Instead, it relies on luminal Ca2+ sensitizing Ca2+ release channels to cytosolic Ca2+.

关键词：算法麻醉药局部/药理学苯胺化合物咖啡因/药理学钙/代谢钙/生理学钙转运atp酶类/拮抗剂和抑制剂中枢神经系统刺激剂/药理学计算机模拟胞质溶胶/药物作用胞质溶胶/代谢电生理学酶抑制剂/药理学荧光染料心脏/药物作用心脏/生理学脂双层显微镜检查共焦模型生物学心肌/细胞学心肌/代谢大鼠 Sprague-Dawley 肌浆网/药物作用肌浆网/代谢毒胡萝卜内酯/药理学呫吨类动物大鼠

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On the characterisation of the mechanism underlying passive activation of the Ca²⁺ release-activated Ca²⁺ current I_CRAC in rat basophilic leukaemia cells

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第2期520卷 407-416页

作者： Fierro, L Parekh, AB Univ Oxford Dept Physiol Lab Mol & Cellular Signalling Oxford OX1 3PT England

1. Tight-seal whole-cell patch clamp experiments were performed to investigate the mechanism whereby passive depletion of stores activates the Ca2+ release-activated Ca2+ current I-CRAC in rat basophilic leukaemia (RBL) cells. 2. Passive depletion of stores was achieved Ly dialysing cells with different concentrations of Ca2+ chelators. Low concentrations generally evoked a submaximal I-CRAC which developed slowly and monophasically. Higher concentrations resulted in a biphasic current in which the initial slow monophasic component developed into a faster and bigger second phase. 3. The kinetics of I-CRAC as well as its final amplitude were not affected by Ca2+ chelators that had different affinities or speeds of binding. *** Ca2+ binding ratios greater than or equal to 16 670 were necessary to fully activate I-CRAC. Because the Ca2+ binding ratio within the stores is presumably lon, this indicates that other factors like Ca2+ transport across the stores membrane are rate limiting for passive store depletion. 5. Heparin and Ruthenium Red both failed to affect passive Ca2+ leak from the intracellular stores. 6. Treatment with sarco/endoplasmic reticulum Ca2+-atpase (SERCA) pump blockers dramatically altered the kinetics of activation of biphasic currents, and increased the amplitude of monophasic ones. 7. Our results suggest that SERCA pumps are very effective in preventing I-CRAC from activating passively, and are responsible for the phasic nature of the current, its time course of development and its overall extent.

关键词：钙/代谢钙通道阻滞药/药理学钙通道/代谢钙转运atp酶类/拮抗剂和抑制剂螯合剂/药理学依他酸/类似物和衍生物依他酸/药理学肝素/药理学吲哚类/药理学白血病嗜碱粒细胞急性膜片钳术蛋白质结合钌红肿瘤细胞培养的动物大鼠

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Bcl-2 and Bcl-X_L block thapsigargin-induced nitric oxide generation, c-Jun NH₂-terminal kinase activity, and apoptosis

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MOLECULAR AND CELLULAR BIOLOGY 1999年第8期19卷 5659-5674页

作者： Srivastava, RK Sollott, SJ Khan, L Hansford, R Lakatta, EG Longo, DL NIA Immunol Lab Intramural Res Program NIH Baltimore MD 21224 USA NIA Lab Cardiovasc Sci Intramural Res Program NIH Baltimore MD 21224 USA NIA Genet Mol Lab Intramural Res Program NIH Baltimore MD 21224 USA

The proteins Bcl-2 and Bcl-X-L prevent apoptosis, but their mechanism of action is unclear. We examined the role of Bcl-2 and Bcl-X-L in the regulation of cytosolic Ca2+, nitric oxide production (NO), c-Jun NH2-terminal kinase (JNK) activation, and apoptosis in Jurkat T cells. Thapsigargin (TG), an inhibitor of the endoplasmic reticulum-associated Ca2+ atpase, was used to disrupt Ca2+ homeostasis. TG acutely elevated intracellular free Ca2+ and mitochondrial Ca2+ levels and induced NO production and apoptosis in Jurkat cells transfected with vector (JT/Neo). Buffering of this Ca2+ response with 1,2-bis (o-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA-AM) or inhibiting NO synthase activity with N-G-nitro-L-arginine methyl ester hydrochloride (L-NAR IE) blocked TG-induced NO production and apoptosis in JT/Neo cells. By contrast, while TG produced comparable early changes in the Ca2+ level (i.e., within 3 h) in Jurkat cells overexpressing Bcl-2 and Bcl-X-L (JT/Bcl-2 or JT/Bcl-X-L), NO production, late (36-h) Ca2+ accumulation, and apoptosis were dramatically reduced compared to those in JT/Neo cells. Exposure of JT/Bcl-2 and JT/Bcl-X-L, cells to the NO donor, S-nitroso-N-acetylpenacillamine (SNAP) resulted in apoptosis comparable to that seen in JT/Neo cells. TG also activated the JNK pathway, which was blocked by L-NAME. Transient expression of a dominant negative mutant SEK1 (Lys --> Arg), an upstream kinase of JNK, prevented both TG-induced JNK activation and apoptosis. A dominant negative c-Jun mutant also reduced TG-induced apoptosis. Overexpression of Bcl-2 or Bcl-X-L inhibited TG-induced loss in mitochondrial membrane potential, release of cytochrome c, and activation of caspase-3 and JNK. Inhibition of caspase-3 activation blocked TG-induced JNK activation, suggesting that JNK activation occurred downstream of caspase-3. Thus, TG-induced Ca2+ release leads to NO generation followed by mitochondrial changes including cytochrom

关键词：细胞凋亡/药物作用钙信号/药物作用钙-钙调素依赖性蛋白激酶类/拮抗剂和抑制剂钙-钙调素依赖性蛋白激酶类/遗传学钙转运atp酶类/拮抗剂和抑制剂半胱氨酸天冬氨酸蛋白酶3 半胱氨酸天冬氨酸蛋白酶/代谢半胱氨酸蛋白酶抑制剂/药理学依他酸/类似物和衍生物依他酸/药理学酶激活/药物作用 JNK丝裂原活化蛋白激酶类 Jurkat细胞线粒体/药物作用线粒体/代谢丝裂原激活蛋白激酶类肿瘤蛋白质类/代谢一氧化氮/生物合成一氧化氮供体/药理学一氧化氮合酶/代谢一氧化氮合酶Ⅱ型寡肽类/药理学青霉胺/类似物和衍生物青霉胺/药理学原癌基因蛋白质c-bcl-2/生理学毒胡萝卜内酯/拮抗剂和抑制剂 bcl-X蛋白质人类

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Stimulation of Ca²⁺-independent exocytosis in rat pituitary gonadotrophs by G-protein

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JOURNAL OF PHYSIOLOGY-LONDON 2000年第1期526卷 99-108页

作者： Tse, FW Tse, A Univ Alberta Dept Pharmacol Edmonton AB T6G 2H7 Canada Univ Alberta Div Neurosci Edmonton AB T6G 2H7 Canada

1. We employed the whole-cell recording technique in conjunction with fluorometry to measure cytosolic Ca2+ concentration ([Ca2+],) and exocytosis (capacitance measurement) in single, identified rat gonadotrophs. 2. Direct activation of G-protein (via intracellular dialysis of non-hydrolysable analogues of GTP, but not of GDP) triggered a slow rise in capacitance even in the presence of a fast intracellular Ca2+ chelator. 3. The head-spectrum kinase inhibitors H7 and staurosporine did not prevent this Ca2+- independent exocytosis, ruling out the involvement of the cAMP and PKC pathways. 4. AIF(4)(-);a potent stimulator of heterotrimeric G-proteins, failed to stimulate any exocytosis when the intracellular Ca2+ store was depleted, implicating the involvement of AIF(4)(-)- insensitive G-protein(s). 5. Maximal stimulation of Ca2+-independent exocytosis by GTP analogues did not reduce the number of readily releasable granules that were available subsequently for Ca2+-dependent release. 6. The last finding raises the possibility that the G-protein-stimulated Ca2+-independent exocytosis may regulate a pool of granules that is distinct fr om the Ca2+-dependent pool.

关键词： 1-(5-异喹啉磺酰基)-2-甲基哌嗪/药理学铝化合物/药理学钙/代谢钙转运atp酶类/拮抗剂和抑制剂环AMP/代谢细胞质颗粒/药物作用细胞质颗粒/代谢胞质溶胶/代谢依他酸/类似物和衍生物依他酸/药理学酶抑制剂/药理学胞吐作用/药物作用胞吐作用/生理学氟化物/药理学荧光计 GTP结合蛋白质类/代谢 GTP结合蛋白质类/药理学鸟苷5'-O-(3-硫代三磷酸)/药理学鸟苷酰亚胺二磷酸/药理学膜片钳术光解垂体前叶/细胞学垂体前叶/药物作用垂体前叶/代谢蛋白激酶C/拮抗剂和抑制剂星状孢子素/药理学动物男(雄)性大鼠

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Calcium release from internal stores is required for the generation of spontaneous hyperpolarizations in dopaminergic neurons of neonatal rats

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JOURNAL OF NEUROPHYSIOLOGY 2000年第1期83卷 192-197页

作者： Seutin, V Mkahli, F Massotte, L Dresse, P Univ Liege Pharmacol Lab Tour Pathol B23 B-4000 Sart I Belgium

We recently have demonstrated the existence of spontaneous hyperpolarizations in midbrain dopaminergic neurons of neonatal but not adult rats. These events are mediated by the opening of apamin-sensitive K+ channels after a rise in the intracellular concentration of Ca2+ They are resistant to tetrodotoxin in most cases and are probably endogenous (i.e., not synaptically activated). Here their mechanism was investigated. Cyclopiazonic acid (10 mu M), a specific inhibitor of endoplasmic reticulum Ca2+ atpases, reversibly abolished the events. Caffeine, which promotes Ca2+ release from intracellular stores, had concentration-dependent effects. At 1 mM, it markedly and steadily increased the frequency and the amplitude of the hyperpolarizations. At 10 mM, it induced a transient increase in their frequency followed by their cessation. All these effects were quickly reversible. Ryanodine (10 mu M), which decreases the conductance of Ca2+ release channels, irreversibly blocked the spontaneous hyperpolarizations. Dantrolene (100 mu M), a blocker of Ca2+ release from sarcoplasmic reticulum of striated muscle, did not affect the events. On the other hand, Cd2+ (100-300 mu M), a broad antagonist of membrane voltage-gated Ca2+ channels, significantly reduced the amplitude and the frequency of the hyperpolarizations. However, when the frequency of the events was increased by 1 mM, caffeine, Cd2+ affected them to a smaller extent, whereas cyclopiazonic acid still abolished them. We conclude that internal stores are the major source of Ca2+ ions that induce the K+ channel openings underlying the spontaneous hyperpolarizations of these neurons.

关键词：动物新生蜂毒明肽/药理学脑/生理学咖啡因/药理学钙/代谢钙转运atp酶类/拮抗剂和抑制剂丹曲林/药理学多巴胺/生理学酶抑制剂/药理学诱发电位/药物作用吲哚类/药理学神经元/药物作用神经元/生理学大鼠 Sprague-Dawley 大鼠 Wistar 兰尼碱/药理学动物大鼠

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Interactions of 6-gingerol and ellagic acid with the cardiac sarcoplasmic reticulum Ca²⁺-atpase

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期290卷 227-234页

作者： Antipenko, AY Spielman, AI Kirchberger, MA CUNY Mt Sinai Sch Med Dept Phys & Biophys New York NY 10029 USA

The inotropic/lusitropic effects of p-adrenergic agonists on the heart are mediated largely by protein kinase A (PKA)-catalyzed phosphorylation of phospholamban, the natural protein regulator of the Ca2+ pump present in sarcoplasmic reticulum (SR) membranes. Gingerol, a plant derivative, is known to produce similar effects when tested in isolated cardiac muscle. The purpose of the present study was to compare the effects of gingerol and another plant derivative, ellagic acid, on the kinetics of the SR Ca2+ pump with those of PKA-catalyzed phospholamban phosphorylation to elucidate their mechanisms of Ca2+ pump regulation. As previously demonstrated for PKA, 50 mu M gingerol or ellagic acid increased V-max(Ca) of Ca2+ uptake and Ca2+-atpase activity assayed at millimolar atp concentrations in light cardiac SR vesicles. Unlike PKA, which decreases K-m(Ca), neither compound had a significant effect on K-m(Ca) in unphosphorylated vesicles. However, gingerol increased K-m(Ca) in phosphorylated vesicles, in which Ca2+ uptake was significantly increased further at saturating Ca2+ and remained unchanged at subsaturating Ca2+. An inhibition of Ca2+ uptake by gingerol at micromolar Mgatp concentrations was overcome with increasing Mgatp concentrations. The stimulation of Ca2+ uptake attributable to gingerol in unphosphorylated microsomes at saturating Ca2+ was 30% to 40% when assayed at 0.05 to 2 mM Mgatp and only about 12% in phosphorylated microsomes as well as in rabbit fast skeletal muscle light SR. The present results support the view that an atp-dependent increase in V-max(Ca) of the SR Ca2+ pump plays an important role in mediating cardiac contractile responses to gingerol and phospholamban-dependent beta-adrenergic stimulation.

关键词：钙/代谢钙转运atp酶类/拮抗剂和抑制剂钙转运atp酶类/代谢环AMP依赖性蛋白激酶类/代谢鞣花酸/药理学脂肪族醇类/药理学草药-药物相互作用动力学微粒体/药物作用微粒体/酶学肌骨骼/药物作用肌骨骼/酶学肌骨骼/超微结构心肌/酶学心肌/代谢心肌/超微结构磷酸盐类/代谢磷酰化植物药用肌浆网/药物作用肌浆网/酶学动物狗兔

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