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  1. AU="Picht, Eckard"
  2. AU="Olvera-Sosa, Miguel"
  3. AU="Kent, N"
  4. AU=Simon Junior Hany AU=Simon Junior Hany
  5. AU="Stevens-Hernandez, Christian J"
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  7. AU="Odenigbo, Kenechukwu A"
  8. AU="Dana N. Mitzel"
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  14. AU="Hougaard, Anders"
  15. AU="Da Cruz ESilva, C Beir Ao"
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  17. AU="Frost, Patrice A"
  18. AU="Nielsen, David R"
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  20. AU="Ziv Ben-Ari"
  21. AU="Gönen, Murat"
  22. AU="Soliman, Essam S"
  23. AU="Poenisch, Falk"
  24. AU="Ng C."
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  1. Artikel: Klinische Studien: Die Deutsche Forschungsgemeinschaft hat das Förderprogramm "Klinische Studien" erweitert. Bisher wurden rund 39 Millionen Euro für Studien aus allen Bereichen der Medizin und Psychologie neu bewilligt

    Großmann, Katja / Picht, Eckard

    Deutsches Ärzteblatt : Ausgabe A, Praxis-Ausgabe : niedergelassene Ärzte

    2018  Band 115, Heft 5, Seite(n) 188

    Sprache Deutsch
    Dokumenttyp Artikel
    ZDB-ID 1453475-7
    ISSN 0012-1207
    Datenquelle Current Contents Medizin

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  2. Artikel ; Online: Mitochondrial free calcium regulation during sarcoplasmic reticulum calcium release in rat cardiac myocytes.

    Andrienko, Tatyana N / Picht, Eckard / Bers, Donald M

    Journal of molecular and cellular cardiology

    2009  Band 46, Heft 6, Seite(n) 1027–1036

    Abstract: Cardiac mitochondria can take up Ca(2+), competing with Ca(2+) transporters like the sarcoplasmic reticulum (SR) Ca(2+)-ATPase. Rapid mitochondrial [Ca(2+)] transients have been reported to be synchronized with normal cytosolic [Ca(2+)](i) transients. ... ...

    Abstract Cardiac mitochondria can take up Ca(2+), competing with Ca(2+) transporters like the sarcoplasmic reticulum (SR) Ca(2+)-ATPase. Rapid mitochondrial [Ca(2+)] transients have been reported to be synchronized with normal cytosolic [Ca(2+)](i) transients. However, most intra-mitochondrial free [Ca(2+)] ([Ca(2+)](mito)) measurements have been uncalibrated, and potentially contaminated by non-mitochondrial signals. Here we measured calibrated [Ca(2+)](mito) in single rat myocytes using the ratiometric Ca(2+) indicator fura-2 AM and plasmalemmal permeabilization by saponin (to eliminate cytosolic fura-2). The steady-state [Ca(2+)](mito) dependence on [Ca(2+)](i) (with 5 mM EGTA) was sigmoid with [Ca(2+)](mito)<[Ca(2+)](i) for [Ca(2+)](i) below 475 nM. With low [EGTA] (50 microM) and 150 nM [Ca(2+)](i) (+/-15 mM Na(+)) cyclical spontaneous SR Ca(2+) release occurred (5-15/min). Changes in [Ca(2+)](mito) during individual [Ca(2+)](i) transients were small ( approximately 2-10 nM/beat), but integrated gradually to steady-state. Inhibition SR Ca(2+) handling by thapsigargin, 2 mM tetracaine or 10 mM caffeine all stopped the progressive rise in [Ca(2+)](mito) and spontaneous Ca(2+) transients (confirming that SR Ca(2+) releases caused the [Ca(2+)](mito) rise). Confocal imaging of local [Ca(2+)](mito) (using rhod-2) showed that [Ca(2+)](mito) rose rapidly with a delay after SR Ca(2+) release (with amplitude up to 10 nM), but declined much more slowly than [Ca(2+)](i) (time constant 2.8+/-0.7 s vs. 0.19+/-0.06 s). Total Ca(2+) uptake for larger [Ca(2+)](mito) transients was approximately 0.5 micromol/L cytosol (assuming 100:1 mitochondrial Ca(2+) buffering), consistent with prior indirect estimates from [Ca(2+)](i) measurements, and corresponds to approximately 1% of the SR Ca(2+) uptake during a normal Ca(2+) transient. Thus small phasic [Ca(2+)](mito) transients and gradually integrating [Ca(2+)](mito) signals occur during repeating [Ca(2+)](i) transients.
    Mesh-Begriff(e) Anesthetics, Local/pharmacology ; Animals ; Biological Transport/drug effects ; Biological Transport/physiology ; Caffeine/pharmacology ; Calcium/metabolism ; Enzyme Inhibitors/pharmacology ; Kinetics ; Male ; Microscopy, Fluorescence ; Mitochondria, Heart/metabolism ; Myocytes, Cardiac/metabolism ; Phosphodiesterase Inhibitors/pharmacology ; Rats ; Rats, Sprague-Dawley ; Sarcoplasmic Reticulum/metabolism ; Tetracaine/pharmacology ; Thapsigargin/pharmacology
    Chemische Substanzen Anesthetics, Local ; Enzyme Inhibitors ; Phosphodiesterase Inhibitors ; Tetracaine (0619F35CGV) ; Caffeine (3G6A5W338E) ; Thapsigargin (67526-95-8) ; Calcium (SY7Q814VUP)
    Sprache Englisch
    Erscheinungsdatum 2009-04-01
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2009.03.015
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Termination of cardiac Ca2+ sparks: role of intra-SR [Ca2+], release flux, and intra-SR Ca2+ diffusion.

    Zima, Aleksey V / Picht, Eckard / Bers, Donald M / Blatter, Lothar A

    Circulation research

    2008  Band 103, Heft 8, Seite(n) e105–15

    Abstract: Ca(2+) release from cardiac sarcoplasmic reticulum (SR) via ryanodine receptors (RyRs) is regulated by dyadic cleft [Ca(2+)] and intra-SR free [Ca(2+)] ([Ca(2+)](SR)). Robust SR Ca(2+) release termination is important for stable excitation-contraction ... ...

    Abstract Ca(2+) release from cardiac sarcoplasmic reticulum (SR) via ryanodine receptors (RyRs) is regulated by dyadic cleft [Ca(2+)] and intra-SR free [Ca(2+)] ([Ca(2+)](SR)). Robust SR Ca(2+) release termination is important for stable excitation-contraction coupling, and partial [Ca(2+)](SR) depletion may contribute to release termination. Here, we investigated the regulation of SR Ca(2+) release termination of spontaneous local SR Ca(2+) release events (Ca(2+) sparks) by [Ca(2+)](SR), release flux, and intra-SR Ca(2+) diffusion. We simultaneously measured Ca(2+) sparks and Ca(2+) blinks (localized elementary [Ca(2+)](SR) depletions) in permeabilized ventricular cardiomyocytes over a wide range of SR Ca(2+) loads and release fluxes. Sparks terminated via a [Ca(2+)](SR)-dependent mechanism at a fixed [Ca(2+)](SR) depletion threshold independent of the initial [Ca(2+)](SR) and release flux. Ca(2+) blink recovery depended mainly on intra-SR Ca(2+) diffusion rather than SR Ca(2+) uptake. Therefore, the large variation in Ca(2+) blink recovery rates at different release sites occurred because of differences in the degree of release site interconnection within the SR network. When SR release flux was greatly reduced, long-lasting release events occurred from well-connected junctions. These junctions could sustain release because local SR Ca(2+) release and [Ca(2+)](SR) refilling reached a balance, preventing [Ca(2+)](SR) from depleting to the termination threshold. Prolonged release events eventually terminated at a steady [Ca(2+)](SR), indicative of a slower, [Ca(2+)](SR)-independent termination mechanism. These results demonstrate that there is high variability in local SR connectivity but that SR Ca(2+) release terminates at a fixed [Ca(2+)](SR) termination threshold. Thus, reliable SR Ca(2+) release termination depends on tight RyR regulation by [Ca(2+)](SR).
    Mesh-Begriff(e) Animals ; Calcium Channel Blockers/pharmacology ; Calcium Signaling/drug effects ; Diffusion ; Heart Ventricles/metabolism ; In Vitro Techniques ; Kinetics ; Membrane Potentials ; Microscopy, Fluorescence ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/enzymology ; Myocytes, Cardiac/metabolism ; Permeability ; Rabbits ; Ryanodine Receptor Calcium Release Channel/drug effects ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/drug effects ; Sarcoplasmic Reticulum/enzymology ; Sarcoplasmic Reticulum/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism
    Chemische Substanzen Calcium Channel Blockers ; Ryanodine Receptor Calcium Release Channel ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8)
    Sprache Englisch
    Erscheinungsdatum 2008-09-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.107.183236
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: SparkMaster: automated calcium spark analysis with ImageJ.

    Picht, Eckard / Zima, Aleksey V / Blatter, Lothar A / Bers, Donald M

    American journal of physiology. Cell physiology

    2007  Band 293, Heft 3, Seite(n) C1073–81

    Abstract: Ca sparks are elementary Ca-release events from intracellular Ca stores that are observed in virtually all types of muscle. Typically, Ca sparks are measured in the line-scan mode with confocal laser-scanning microscopes, yielding two-dimensional images ( ...

    Abstract Ca sparks are elementary Ca-release events from intracellular Ca stores that are observed in virtually all types of muscle. Typically, Ca sparks are measured in the line-scan mode with confocal laser-scanning microscopes, yielding two-dimensional images (distance vs. time). The manual analysis of these images is time consuming and prone to errors as well as investigator bias. Therefore, we developed SparkMaster, an automated analysis program that allows rapid and reliable spark analysis. The underlying analysis algorithm is adapted from the threshold-based standard method of spark analysis developed by Cheng et al. (Biophys J 76: 606-617, 1999) and is implemented here in the freely available image-processing software ImageJ. SparkMaster offers a graphical user interface through which all analysis parameters and output options are selected. The analysis includes general image parameters (number of detected sparks, spark frequency) and individual spark parameters (amplitude, full width at half-maximum amplitude, full duration at half-maximum amplitude, full width, full duration, time to peak, maximum steepness of spark upstroke, time constant of spark decay). We validated the algorithm using images with synthetic sparks embedded into backgrounds with different signal-to-noise ratios to determine an analysis criteria at which a high sensitivity is combined with a low frequency of false-positive detections. Finally, we applied SparkMaster to analyze experimental data of sparks measured in intact and permeabilized ventricular cardiomyocytes, permeabilized mammalian skeletal muscle, and intact smooth muscle cells. We found that SparkMaster provides a reliable, easy to use, and fast way of analyzing Ca sparks in a wide variety of experimental conditions.
    Mesh-Begriff(e) Algorithms ; Animals ; Calcium/metabolism ; Calcium Signaling/physiology ; Cats ; Female ; Male ; Mice ; Microscopy, Confocal/instrumentation ; Microscopy, Confocal/methods ; Microscopy, Confocal/standards ; Muscle Fibers, Skeletal/metabolism ; Myocytes, Cardiac/metabolism ; Myocytes, Smooth Muscle/metabolism ; Predictive Value of Tests ; Reproducibility of Results ; Sarcoplasmic Reticulum/metabolism ; Software
    Chemische Substanzen Calcium (SY7Q814VUP)
    Sprache Englisch
    Erscheinungsdatum 2007-03-21
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00586.2006
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Partial inhibition of sarcoplasmic reticulum ca release evokes long-lasting ca release events in ventricular myocytes: role of luminal ca in termination of ca release.

    Zima, Aleksey V / Picht, Eckard / Bers, Donald M / Blatter, Lothar A

    Biophysical journal

    2007  Band 94, Heft 5, Seite(n) 1867–1879

    Abstract: In cardiac myocytes, local sarcoplasmic reticulum (SR) Ca depletion during Ca sparks is believed to play an important role in the termination of SR Ca release. We tested whether decreasing the rate of SR Ca depletion by partially inhibiting SR Ca release ...

    Abstract In cardiac myocytes, local sarcoplasmic reticulum (SR) Ca depletion during Ca sparks is believed to play an important role in the termination of SR Ca release. We tested whether decreasing the rate of SR Ca depletion by partially inhibiting SR Ca release channels (ryanodine receptors) delays Ca spark termination. In permeabilized cat ventricular myocytes, 0.7 mM tetracaine caused almost complete Ca spark inhibition followed by a recovery significantly below control level. The recovery was associated with increased SR Ca load and increased Ca spark duration. Additionally, SR Ca release events lasting several hundred milliseconds occurred consistently. These events had a significantly lower initial Ca release flux followed by a stable plateau, indicating delayed release termination and maintained SR Ca load. Increasing SR Ca load (without inhibiting SR Ca release rate) or decreasing SR Ca release rate (without increasing SR Ca load) both induced only a small increase in spark duration. These results show that the combination of decreased release flux and increased SR Ca load has synergistic effects and exerts major changes on the termination of Ca release events. Long-lasting Ca release events may originate from highly interconnected release junctions where Ca diffusion from neighboring sites partially compensates Ca depletion, thereby delaying SR Ca-dependent termination. Eventually, these events terminate by luminal Ca-independent mechanisms, such as inactivation, adaptation, or stochastic attrition.
    Mesh-Begriff(e) Anesthetics, Local/pharmacology ; Animals ; Calcium/metabolism ; Calcium Signaling/physiology ; Cats ; Heart Ventricles/cytology ; Heart Ventricles/drug effects ; Heart Ventricles/metabolism ; Kinetics ; Ryanodine Receptor Calcium Release Channel/drug effects ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/drug effects ; Sarcoplasmic Reticulum/metabolism ; Tetracaine/pharmacology
    Chemische Substanzen Anesthetics, Local ; Ryanodine Receptor Calcium Release Channel ; Tetracaine (0619F35CGV) ; Calcium (SY7Q814VUP)
    Sprache Englisch
    Erscheinungsdatum 2007-11-16
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 218078-9
    ISSN 1542-0086 ; 0006-3495
    ISSN (online) 1542-0086
    ISSN 0006-3495
    DOI 10.1529/biophysj.107.114694
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Cardiac alternans do not rely on diastolic sarcoplasmic reticulum calcium content fluctuations.

    Picht, Eckard / DeSantiago, Jaime / Blatter, Lothar A / Bers, Donald M

    Circulation research

    2006  Band 99, Heft 7, Seite(n) 740–748

    Abstract: Cardiac alternans are thought to be a precursor to life-threatening arrhythmias. Previous studies suggested that alterations in sarcoplasmic reticulum (SR) Ca2+ content are either causative or not associated with myocyte Ca2+ alternans. However, those ... ...

    Abstract Cardiac alternans are thought to be a precursor to life-threatening arrhythmias. Previous studies suggested that alterations in sarcoplasmic reticulum (SR) Ca2+ content are either causative or not associated with myocyte Ca2+ alternans. However, those studies used indirect measures of SR Ca2+. Here we used direct continuous measurement of intra-SR free [Ca2+] ([Ca2+]SR) (using Fluo5N) during frequency-dependent Ca2+ alternans in rabbit ventricular myocytes. We tested the hypothesis that alternating [Ca2+]SR is required for Ca2+ alternans. Amplitudes of [Ca2+]SR depletions alternated in phase with cytosolic Ca2+ transients and contractions. Some cells showed clear alternation in diastolic [Ca2+]SR during alternans, with higher [Ca2+]SR before the larger SR Ca2+ releases. However, the extent of SR Ca2+ release during the small beats was smaller than expected for the modest decrease in [Ca2+]SR. In other cells, clear Ca2+ alternans was observed without alternations in diastolic [Ca2+]SR. Additionally, alternating cells were observed, in which diastolic [Ca2+]SR fluctuations occurred interspersed by depletions in which the amplitude was unrelated to the preceding diastolic [Ca2+]SR. In all forms of alternans, the SR Ca2+ release rate was higher during large depletions than during small depletions. Although [Ca2+]SR exerts major influence on SR Ca2+ release, alternations in [Ca2+](SR) are not required for Ca2+ alternans to occur. Rather, it seems likely that some other factor, such as ryanodine receptor availability after a prior beat (eg, recovery from inactivation), is of greater importance in initiating frequency-induced Ca2+ alternans. However, once such a weak SR Ca2+ release occurs, it can result in increased [Ca2+]SR and further enhance SR Ca2+ release at the next beat. In this way, diastolic [Ca2+]SR alternans can enhance frequency-induced Ca2+ alternans, even if they initiate by other means.
    Mesh-Begriff(e) Animals ; Arrhythmias, Cardiac/metabolism ; Arrhythmias, Cardiac/physiopathology ; Calcium/metabolism ; Calcium Channels, L-Type/metabolism ; Diastole ; Heart Ventricles ; Intracellular Membranes/metabolism ; Myocytes, Cardiac/metabolism ; Osmolar Concentration ; Pulse ; Rabbits ; Sarcoplasmic Reticulum/metabolism ; Time Factors
    Chemische Substanzen Calcium Channels, L-Type ; Calcium (SY7Q814VUP)
    Sprache Englisch
    Erscheinungsdatum 2006-09-29
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/01.RES.0000244002.88813.91
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Dynamic calcium movement inside cardiac sarcoplasmic reticulum during release.

    Picht, Eckard / Zima, Aleksey V / Shannon, Thomas R / Duncan, Alexis M / Blatter, Lothar A / Bers, Donald M

    Circulation research

    2011  Band 108, Heft 7, Seite(n) 847–856

    Abstract: Rationale: Intra-sarcoplasmic reticulum (SR) free [Ca] ([Ca](SR)) provides the driving force for SR Ca release and is a key regulator of SR Ca release channel gating during normal SR Ca release or arrhythmogenic spontaneous Ca release events. However, ... ...

    Abstract Rationale: Intra-sarcoplasmic reticulum (SR) free [Ca] ([Ca](SR)) provides the driving force for SR Ca release and is a key regulator of SR Ca release channel gating during normal SR Ca release or arrhythmogenic spontaneous Ca release events. However, little is known about [Ca](SR) spatiotemporal dynamics.
    Objective: To directly measure local [Ca](SR) with subsarcomeric spatiotemporal resolution during both normal global SR Ca release and spontaneous Ca sparks and to evaluate the quantitative implications of spatial [Ca](SR) gradients.
    Methods and results: Intact and permeabilized rabbit ventricular myocytes were subjected to direct simultaneous measurement of cytosolic [Ca] and [Ca](SR) and FRAP (fluorescence recovery after photobleach). We found no detectable [Ca](SR) gradients between SR release sites (junctional SR) and Ca uptake sites (free SR) during normal global Ca release, clear spatiotemporal [Ca](SR) gradients during isolated Ca blinks, faster intra-SR diffusion in the longitudinal versus transverse direction, 3- to 4-fold slower diffusion of fluorophores in the SR than in cytosol, and that intra-SR Ca diffusion varies locally, dependent on local SR connectivity. A computational model clarified why spatiotemporal gradients are more detectable in isolated local releases versus global releases and provides a quantitative framework for understanding intra-SR Ca diffusion.
    Conclusions: Intra-SR Ca diffusion is rapid, limiting spatial [Ca](SR) gradients during excitation-contraction coupling. Spatiotemporal [Ca](SR) gradients are apparent during Ca sparks, and these observations constrain models of dynamic Ca movement inside the SR. This has important implications for myocyte SR Ca handling, synchrony, and potentially arrhythmogenic spontaneous contraction.
    Mesh-Begriff(e) Animals ; Calcium/metabolism ; Calcium Channels/metabolism ; Calcium Signaling/physiology ; Cells, Cultured ; Models, Animal ; Models, Theoretical ; Muscle Contraction/physiology ; Myocardium/cytology ; Myocardium/metabolism ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/metabolism ; Rabbits ; Sarcoplasmic Reticulum/metabolism
    Chemische Substanzen Calcium Channels ; Calcium (SY7Q814VUP)
    Sprache Englisch
    Erscheinungsdatum 2011-02-10
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.111.240234
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Kinetics of FKBP12.6 binding to ryanodine receptors in permeabilized cardiac myocytes and effects on Ca sparks.

    Guo, Tao / Cornea, Razvan L / Huke, Sabine / Camors, Emmanuel / Yang, Yi / Picht, Eckard / Fruen, Bradley R / Bers, Donald M

    Circulation research

    2010  Band 106, Heft 11, Seite(n) 1743–1752

    Abstract: Rationale: FK506-binding proteins FKBP12.6 and FKBP12 are associated with cardiac ryanodine receptors (RyR2), and cAMP-dependent protein kinase A (PKA)-dependent phosphorylation of RyR2 was proposed to interrupt FKBP12.6-RyR2 association and activate ... ...

    Abstract Rationale: FK506-binding proteins FKBP12.6 and FKBP12 are associated with cardiac ryanodine receptors (RyR2), and cAMP-dependent protein kinase A (PKA)-dependent phosphorylation of RyR2 was proposed to interrupt FKBP12.6-RyR2 association and activate RyR2. However, the function of FKBP12.6/12 and role of PKA phosphorylation in cardiac myocytes are controversial.
    Objective: To directly measure in situ binding of FKBP12.6/12 to RyR2 in ventricular myocytes, with simultaneous Ca sparks measurements as a RyR2 functional index.
    Methods and results: We used permeabilized rat and mouse ventricular myocytes, and fluorescently-labeled FKBP12.6/12. Both FKBP12.6 and FKBP12 concentrate at Z-lines, consistent with RyR2 and Ca spark initiation sites. However, only FKBP12.6 inhibits resting RyR2 activity. Assessment of fluorescent FKBP binding in myocyte revealed a high FKBP12.6-RyR2 affinity (K(d)=0.7+/-0.1 nmol/L) and much lower FKBP12-RyR2 affinity (K(d)=206+/-70 nmol/L). Fluorescence recovery after photobleach confirmed this K(d) difference and showed that it is mediated by k(off). RyR2 phosphorylation by PKA did not alter binding kinetics or affinity of FKBP12.6/12 for RyR2. Using quantitative immunoblots, we determined endogenous [FKBP12] in intact myocytes is approximately 1 micromol/L (similar to [RyR]), whereas [FKBP12.6] is <or=150 nmol/L.<br />Conclusions: Only 10% to 20% of endogenous myocyte RyR2s have FKBP12.6 associated, but virtually all myocyte FKBP12.6 is RyR2-bound (because of very high affinity). FKBP12.6 but not FKBP12 inhibits basal RyR2 activity. PKA-dependent RyR2 phosphorylation has no significant effect on binding of either FKBP12 or 12.6 to RyR2 in myocytes.
    Mesh-Begriff(e) Animals ; Blotting, Western ; Calcium Signaling/drug effects ; Cell Membrane Permeability ; Circular Dichroism ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Fluorescence Recovery After Photobleaching ; Heart Ventricles/metabolism ; Humans ; Kinetics ; Mice ; Mice, Knockout ; Microscopy, Confocal ; Mutagenesis, Site-Directed ; Mutation ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Phosphorylation ; Protein Binding ; Rats ; Ryanodine Receptor Calcium Release Channel/drug effects ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/metabolism ; Sirolimus/pharmacology ; Swine ; Tacrolimus Binding Protein 1A/genetics ; Tacrolimus Binding Protein 1A/metabolism ; Tacrolimus Binding Proteins/deficiency ; Tacrolimus Binding Proteins/genetics ; Tacrolimus Binding Proteins/metabolism
    Chemische Substanzen FKBP12.6 protein, mouse ; Ryanodine Receptor Calcium Release Channel ; Cyclic AMP (E0399OZS9N) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Tacrolimus Binding Protein 1A (EC 5.2.1.-) ; Tacrolimus Binding Proteins (EC 5.2.1.-) ; tacrolimus binding protein 1B (EC 5.2.1.-) ; Sirolimus (W36ZG6FT64)
    Sprache Englisch
    Erscheinungsdatum 2010-04-29
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.110.219816
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Hypercontractile female hearts exhibit increased S-nitrosylation of the L-type Ca2+ channel alpha1 subunit and reduced ischemia/reperfusion injury.

    Sun, Junhui / Picht, Eckard / Ginsburg, Kenneth S / Bers, Donald M / Steenbergen, Charles / Murphy, Elizabeth

    Circulation research

    2006  Band 98, Heft 3, Seite(n) 403–411

    Abstract: Mechanisms underlying gender differences in cardiovascular disease are poorly understood. We found previously that, under hypercontractile conditions, female hearts exhibit significantly less ischemia/reperfusion injury than males. Here we show that male ...

    Abstract Mechanisms underlying gender differences in cardiovascular disease are poorly understood. We found previously that, under hypercontractile conditions, female hearts exhibit significantly less ischemia/reperfusion injury than males. Here we show that male wild-type (WT) mouse hearts pretreated with 10 nmol/L isoproterenol before ischemia exhibited increased injury versus female hearts, but this relative protection in females was absent in eNOS(-/-) and nNOS(-/-) hearts. In isoproterenol-treated female versus male hearts, there was also more endothelial NO synthase (eNOS) associated with cardiomyocyte caveolin-3, and more neuronal NOS (nNOS) translocation to caveolin-3 during ischemia/reperfusion. S-nitrosothiol (SNO) formation was increased in isoproterenol-treated ischemic/reperfused hearts in all mouse genotypes, but only in WT mice was SNO content significantly higher in females than males. Using the biotin switch method, we identified the L-type Ca2+ channel alpha1 subunit as the predominant S-nitrosylated protein in membrane fractions, and following isoproterenol and ischemia/reperfusion male/female differences in SNO were seen only in WT hearts, but not in constitutive NOS(-/-) genotypes. The isoproterenol-induced increase in L-type Ca2+ current (ICa) was smaller in females versus in males, but NOS blockade increased ICa in females. This gender difference in ICa in isoproterenol-treated myocytes (and abolition on NOS inhibition) was mirrored exactly in Ca2+ transients and SR Ca2+ contents. In conclusion, these data suggest that eNOS and nNOS both play roles in the gender differences observed in ischemia/reperfusion injury under adrenergic stimulation, and also demonstrate increased S-nitrosylation of the L-type Ca2+ channels in female cardiomyocytes.
    Mesh-Begriff(e) Animals ; Calcium Channels, L-Type/metabolism ; Cardiotonic Agents/pharmacology ; Female ; Isoproterenol/pharmacology ; Male ; Mice ; Mice, Knockout ; Myocardial Contraction/drug effects ; Myocardial Contraction/physiology ; Myocardial Reperfusion Injury/physiopathology ; Myocardial Reperfusion Injury/prevention & control ; Nitric Oxide Synthase Type I/deficiency ; Nitric Oxide Synthase Type I/genetics ; Nitric Oxide Synthase Type I/metabolism ; Nitric Oxide Synthase Type III/deficiency ; Nitric Oxide Synthase Type III/genetics ; Nitric Oxide Synthase Type III/metabolism ; Sex Characteristics
    Chemische Substanzen Calcium Channels, L-Type ; Cardiotonic Agents ; L-type calcium channel alpha(1C) ; Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Isoproterenol (L628TT009W)
    Sprache Englisch
    Erscheinungsdatum 2006-02-17
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/01.RES.0000202707.79018.0a
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel: CaMKII inhibition targeted to the sarcoplasmic reticulum inhibits frequency-dependent acceleration of relaxation and Ca2+ current facilitation.

    Picht, Eckard / DeSantiago, Jaime / Huke, Sabine / Kaetzel, Marcia A / Dedman, John R / Bers, Donald M

    Journal of molecular and cellular cardiology

    2006  Band 42, Heft 1, Seite(n) 196–205

    Abstract: Cardiac Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in heart has been implicated in Ca(2+) current (I(Ca)) facilitation, enhanced sarcoplasmic reticulum (SR) Ca(2+) release and frequency-dependent acceleration of relaxation (FDAR) via enhanced ...

    Abstract Cardiac Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in heart has been implicated in Ca(2+) current (I(Ca)) facilitation, enhanced sarcoplasmic reticulum (SR) Ca(2+) release and frequency-dependent acceleration of relaxation (FDAR) via enhanced SR Ca(2+) uptake. However, questions remain about how CaMKII may work in these three processes. Here we tested the role of CaMKII in these processes using transgenic mice (SR-AIP) that express four concatenated repeats of the CaMKII inhibitory peptide AIP selectively in the SR membrane. Wild type mice (WT) and mice expressing AIP exclusively in the nucleus (NLS-AIP) served as controls. Increasing stimulation frequency produced typical FDAR in WT and NLS-AIP, but FDAR was markedly inhibited in SR-AIP. Quantitative analysis of cytosolic Ca(2+) removal during [Ca(2+)](i) decline revealed that FDAR is due to an increased apparent V(max) of SERCA. CaMKII-dependent RyR phosphorylation at Ser2815 and SR Ca(2+) leak was both decreased in SR-AIP vs. WT. This decrease in SR Ca(2+) leak may partly balance the reduced SERCA activity leading to relatively unaltered SR-Ca(2+) load in SR-AIP vs. WT myocytes. Surprisingly, CaMKII regulation of the L-type Ca(2+) channel (I(Ca) facilitation and recovery from inactivation) was abolished by the SR-targeted CaMKII inhibition in SR-AIP mice. Inhibition of CaMKII effects on I(Ca) and RyR function by the SR-localized AIP places physical constraints on the localization of these proteins at the junctional microdomain. Thus SR-targeted CaMKII inhibition can directly inhibit the activation of SR Ca(2+) uptake, SR Ca(2+) release and I(Ca) by CaMKII, effects which have all been implicated in triggered arrhythmias.
    Mesh-Begriff(e) Animals ; Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors ; Cytosol/metabolism ; Female ; In Vitro Techniques ; Kinetics ; Male ; Mice ; Mice, Transgenic ; Myocardial Contraction ; Myocytes, Cardiac/metabolism ; Peptides/genetics ; Peptides/metabolism ; Phosphorylation ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism ; Sodium-Calcium Exchanger/metabolism
    Chemische Substanzen CaMKII inhibitor AIP ; Peptides ; Ryanodine Receptor Calcium Release Channel ; Sodium-Calcium Exchanger ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17) ; Calcium-Calmodulin-Dependent Protein Kinases (EC 2.7.11.17) ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8)
    Sprache Englisch
    Erscheinungsdatum 2006-10-17
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2006.09.007
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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