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Seung Woo Lee - One of the best experts on this subject based on the ideXlab platform.

  • noninvasive measurement of electrical events associated with a single chlorovirus infection of a microalgal Cell
    ACS Nano, 2016
    Co-Authors: Gerhard Thiel, Seung Woo Lee, Eun Hee Lee, Ravi F Saraf
    Abstract:

    Chlorovirus Paramecium bursaria chlorella virus 1 (PBCV-1) contains a viral-encoded K+ channel imbedded in its internal Membrane, which triggers host plasma Membrane Depolarization during virus infection. This early stage of infection was monitored at high resolution by recording the Cell Membrane Depolarization of a single Chlorella Cell during infection by a single PBCV-1 particle. The measurement was achieved by depositing the Cells onto a network of one-dimensional necklaces of Au nanoparticles, which spanned two electrodes 70 μm apart. The nanoparticle necklace array has been shown to behave as a single-electron device at room temperature. The resulting electrochemical field-effect transistor (eFET) was gated by the Cell Membrane potential, which allowed a quantitative measurement of the electrophysiological changes across the rigid Cell wall of the microalgae due to a single viral attack at high sensitivity. The single viral infection signature was quantitatively confirmed by coupling the eFET measu...

  • Noninvasive Measurement of Electrical Events Associated with a Single Chlorovirus Infection of a Microalgal Cell
    2016
    Co-Authors: Seung Woo Lee, Gerhard Thiel, Eun Hee Lee, James L. Van Etten, Ravi F Saraf
    Abstract:

    Chlorovirus Paramecium bursaria chlorella virus 1 (PBCV-1) contains a viral-encoded K+ channel imbedded in its internal Membrane, which triggers host plasma Membrane Depolarization during virus infection. This early stage of infection was monitored at high resolution by recording the Cell Membrane Depolarization of a single Chlorella Cell during infection by a single PBCV-1 particle. The measurement was achieved by depositing the Cells onto a network of one-dimensional necklaces of Au nanoparticles, which spanned two electrodes 70 μm apart. The nanoparticle necklace array has been shown to behave as a single-electron device at room temperature. The resulting electrochemical field-effect transistor (eFET) was gated by the Cell Membrane potential, which allowed a quantitative measurement of the electrophysiological changes across the rigid Cell wall of the microalgae due to a single viral attack at high sensitivity. The single viral infection signature was quantitatively confirmed by coupling the eFET measurement with a method in which a single viral particle was delivered for infection by a scanning probe microscope cantilever

Ariel Contreras-ferrat - One of the best experts on this subject based on the ideXlab platform.

  • Mitochondrial calcium increase induced by RyR1 and IP3R channel activation after Membrane Depolarization regulates skeletal muscle metabolism
    Frontiers in physiology, 2018
    Co-Authors: Alexis Díaz-vegas, Alex Cordova, Denisse Valladares, Paola Llanos, Cecilia Hidalgo, Gaia Gherardi, Diego De Stefani, Cristina Mammucari, Rosario Rizzuto, Ariel Contreras-ferrat
    Abstract:

    Aim: We hypothesize that both type-1 ryanodine receptor (RyR1) and IP3-receptor (IP3R) calcium channels are necessary for the mitochondrial Ca2+ increase caused by Membrane Depolarization induced by potassium (or by electrical stimulation) of single skeletal muscle fibers; this calcium increase would couple muscle fiber excitation to an increase in metabolic output from mitochondria (excitation-metabolism coupling). Methods: Mitochondria matrix and cytoplasmic Ca2+ levels were evaluated in fibers isolated from flexor digitorium brevis muscle using plasmids for the expression of a mitochondrial Ca2+ sensor (CEPIA3mt) or a cytoplasmic Ca2+ sensor (RCaMP). The role of intraCellular Ca2+ channels was evaluated using both specific pharmacological inhibitors (xestospongin B for IP3R and Dantrolene for RyR1) and a genetic approach (shIP3R1-RFP). O2 consumption was detected using Seahorse ExtraCellular Flux Analyzer. Results: In isolated muscle fibers Cell Membrane Depolarization increased both cytoplasmic and mitochondrial Ca2+ levels. Mitochondrial Ca2+ uptake required functional inositol IP3R and RyR1 channels. Inhibition of either channel decreased basal O2 consumption rate but only RyR1 inhibition decreased ATP-linked O2 consumption. Cell Membrane Depolarization-induced Ca2+ signals in sub-sarcolemmal mitochondria were accompanied by a reduction in mitochondrial Membrane potential; Ca2+ signals propagated towards intermyofibrillar mitochondria, which displayed increased Membrane potential. These results are compatible with slow, Ca2+-dependent propagation of mitochondrial Membrane potential from the surface towards the center of the fiber. Conclusion: Ca2+-dependent changes in mitochondrial Membrane potential have different kinetics in the surface versus the center of the fiber; these differences are likely to play a critical role in the control of mitochondrial metabolism, both at rest and after Membrane Depolarization as part of an “excitation-metabolism” coupling process in skeletal muscle fibers.

  • Video_3_Mitochondrial Calcium Increase Induced by RyR1 and IP3R Channel Activation After Membrane Depolarization Regulates Skeletal Muscle Metabolism.AVI
    2018
    Co-Authors: Alexis Díaz-vegas, Alex Cordova, Denisse Valladares, Paola Llanos, Cecilia Hidalgo, Gaia Gherardi, Diego De Stefani, Cristina Mammucari, Rosario Rizzuto, Ariel Contreras-ferrat
    Abstract:

    Aim: We hypothesize that both type-1 ryanodine receptor (RyR1) and IP3-receptor (IP3R) calcium channels are necessary for the mitochondrial Ca2+ increase caused by Membrane Depolarization induced by potassium (or by electrical stimulation) of single skeletal muscle fibers; this calcium increase would couple muscle fiber excitation to an increase in metabolic output from mitochondria (excitation-metabolism coupling).Methods: Mitochondria matrix and cytoplasmic Ca2+ levels were evaluated in fibers isolated from flexor digitorium brevis muscle using plasmids for the expression of a mitochondrial Ca2+ sensor (CEPIA3mt) or a cytoplasmic Ca2+ sensor (RCaMP). The role of intraCellular Ca2+ channels was evaluated using both specific pharmacological inhibitors (xestospongin B for IP3R and Dantrolene for RyR1) and a genetic approach (shIP3R1-RFP). O2 consumption was detected using Seahorse ExtraCellular Flux Analyzer.Results: In isolated muscle fibers Cell Membrane Depolarization increased both cytoplasmic and mitochondrial Ca2+ levels. Mitochondrial Ca2+ uptake required functional inositol IP3R and RyR1 channels. Inhibition of either channel decreased basal O2 consumption rate but only RyR1 inhibition decreased ATP-linked O2 consumption. Cell Membrane Depolarization-induced Ca2+ signals in sub-sarcolemmal mitochondria were accompanied by a reduction in mitochondrial Membrane potential; Ca2+ signals propagated toward intermyofibrillar mitochondria, which displayed increased Membrane potential. These results are compatible with slow, Ca2+-dependent propagation of mitochondrial Membrane potential from the surface toward the center of the fiber.Conclusion: Ca2+-dependent changes in mitochondrial Membrane potential have different kinetics in the surface vs. the center of the fiber; these differences are likely to play a critical role in the control of mitochondrial metabolism, both at rest and after Membrane Depolarization as part of an “excitation-metabolism” coupling process in skeletal muscle fibers.

  • Data_Sheet_1_Mitochondrial Calcium Increase Induced by RyR1 and IP3R Channel Activation After Membrane Depolarization Regulates Skeletal Muscle Metabolism.docx
    2018
    Co-Authors: Alexis Díaz-vegas, Alex Cordova, Denisse Valladares, Paola Llanos, Cecilia Hidalgo, Gaia Gherardi, Diego De Stefani, Cristina Mammucari, Rosario Rizzuto, Ariel Contreras-ferrat
    Abstract:

    Aim: We hypothesize that both type-1 ryanodine receptor (RyR1) and IP3-receptor (IP3R) calcium channels are necessary for the mitochondrial Ca2+ increase caused by Membrane Depolarization induced by potassium (or by electrical stimulation) of single skeletal muscle fibers; this calcium increase would couple muscle fiber excitation to an increase in metabolic output from mitochondria (excitation-metabolism coupling).Methods: Mitochondria matrix and cytoplasmic Ca2+ levels were evaluated in fibers isolated from flexor digitorium brevis muscle using plasmids for the expression of a mitochondrial Ca2+ sensor (CEPIA3mt) or a cytoplasmic Ca2+ sensor (RCaMP). The role of intraCellular Ca2+ channels was evaluated using both specific pharmacological inhibitors (xestospongin B for IP3R and Dantrolene for RyR1) and a genetic approach (shIP3R1-RFP). O2 consumption was detected using Seahorse ExtraCellular Flux Analyzer.Results: In isolated muscle fibers Cell Membrane Depolarization increased both cytoplasmic and mitochondrial Ca2+ levels. Mitochondrial Ca2+ uptake required functional inositol IP3R and RyR1 channels. Inhibition of either channel decreased basal O2 consumption rate but only RyR1 inhibition decreased ATP-linked O2 consumption. Cell Membrane Depolarization-induced Ca2+ signals in sub-sarcolemmal mitochondria were accompanied by a reduction in mitochondrial Membrane potential; Ca2+ signals propagated toward intermyofibrillar mitochondria, which displayed increased Membrane potential. These results are compatible with slow, Ca2+-dependent propagation of mitochondrial Membrane potential from the surface toward the center of the fiber.Conclusion: Ca2+-dependent changes in mitochondrial Membrane potential have different kinetics in the surface vs. the center of the fiber; these differences are likely to play a critical role in the control of mitochondrial metabolism, both at rest and after Membrane Depolarization as part of an “excitation-metabolism” coupling process in skeletal muscle fibers.

Reinhold Penner - One of the best experts on this subject based on the ideXlab platform.

  • a pyrazole derivative potently inhibits lymphocyte ca2 influx and cytokine production by facilitating transient receptor potential melastatin 4 channel activity
    Molecular Pharmacology, 2006
    Co-Authors: Ryuichi Takezawa, Jean-pierre Kinet, Pierre Launay, Andrea Fleig, Henrique Cheng, Andreas Beck, Jun Ishikawa, Hirokazu Kubota, Toshimitsu Yamada, Reinhold Penner
    Abstract:

    3,5-Bis(trifluoromethyl)pyrazole derivative (BTP2) or N-[4-3, 5-bis(trifluromethyl)pyrazol-1-yl]-4-methyl-1,2,3-thiadiazole-5-carboxamide (YM-58483) is an immunosuppressive compound that potently inhibits both Ca2+ influx and interleukin-2 (IL-2) production in lymphocytes. We report here that BTP2 dosedependently enhances transient receptor potential melastatin 4 (TRPM4), a Ca2+-activated nonselective (CAN) cation channel that decreases Ca2+ influx by depolarizing lymphocytes. The effect of BTP2 on TRPM4 occurs at low nanomolar concentrations and is highly specific, because other ion channels in T lymphocytes are not significantly affected, and the major Ca2+ influx pathway in lymphocytes, ICRAC, is blocked only at 100-fold higher concentrations. The efficacy of BTP2 in blocking IL-2 production is reduced approximately 100-fold when preventing TRPM4-mediated Membrane Depolarization, suggesting that the BTP2-mediated facilitation of TRPM4 channels represents the major mechanism for its immunosuppressive effect. Our results demonstrate that TRPM4 channels represent a previously unrecognized key element in lymphocyte Ca2+ signaling and that their facilitation by BTP2 supports Cell Membrane Depolarization, which reduces the driving force for Ca2+ entry and ultimately causes the potent suppression of cytokine release.

  • trpm4 is a ca2 activated nonselective cation channel mediating Cell Membrane Depolarization
    Cell, 2002
    Co-Authors: Pierre Launay, Andrea Fleig, Reinhold Penner, Annelaure Perraud, Andrew M Scharenberg, Jean-pierre Kinet
    Abstract:

    Abstract Calcium-activated nonselective (CAN) cation channels are expressed in various excitable and nonexcitable Cells supporting important Cellular responses such as neuronal bursting activity, fluid secretion, and cardiac rhythmicity. We have cloned and characterized a second form of TRPM4, TRPM4b, a member of the TRP channel family, as a molecular candidate of a CAN channel. TRPM4b encodes a cation channel of 25 pS unitary conductance that is directly activated by [Ca 2+ ]i with an apparent K D of ∼400 nM. It conducts monovalent cations such as Na + and K + without significant permeation of Ca 2+ . TRPM4b is activated following receptor-mediated Ca 2+ mobilization, representing a regulatory mechanism that controls the magnitude of Ca 2+ influx by modulating the Membrane potential and, with it, the driving force for Ca 2+ entry through other Ca 2+ -permeable pathways.

Jean-pierre Kinet - One of the best experts on this subject based on the ideXlab platform.

  • a pyrazole derivative potently inhibits lymphocyte ca2 influx and cytokine production by facilitating transient receptor potential melastatin 4 channel activity
    Molecular Pharmacology, 2006
    Co-Authors: Ryuichi Takezawa, Jean-pierre Kinet, Pierre Launay, Andrea Fleig, Henrique Cheng, Andreas Beck, Jun Ishikawa, Hirokazu Kubota, Toshimitsu Yamada, Reinhold Penner
    Abstract:

    3,5-Bis(trifluoromethyl)pyrazole derivative (BTP2) or N-[4-3, 5-bis(trifluromethyl)pyrazol-1-yl]-4-methyl-1,2,3-thiadiazole-5-carboxamide (YM-58483) is an immunosuppressive compound that potently inhibits both Ca2+ influx and interleukin-2 (IL-2) production in lymphocytes. We report here that BTP2 dosedependently enhances transient receptor potential melastatin 4 (TRPM4), a Ca2+-activated nonselective (CAN) cation channel that decreases Ca2+ influx by depolarizing lymphocytes. The effect of BTP2 on TRPM4 occurs at low nanomolar concentrations and is highly specific, because other ion channels in T lymphocytes are not significantly affected, and the major Ca2+ influx pathway in lymphocytes, ICRAC, is blocked only at 100-fold higher concentrations. The efficacy of BTP2 in blocking IL-2 production is reduced approximately 100-fold when preventing TRPM4-mediated Membrane Depolarization, suggesting that the BTP2-mediated facilitation of TRPM4 channels represents the major mechanism for its immunosuppressive effect. Our results demonstrate that TRPM4 channels represent a previously unrecognized key element in lymphocyte Ca2+ signaling and that their facilitation by BTP2 supports Cell Membrane Depolarization, which reduces the driving force for Ca2+ entry and ultimately causes the potent suppression of cytokine release.

  • trpm4 is a ca2 activated nonselective cation channel mediating Cell Membrane Depolarization
    Cell, 2002
    Co-Authors: Pierre Launay, Andrea Fleig, Reinhold Penner, Annelaure Perraud, Andrew M Scharenberg, Jean-pierre Kinet
    Abstract:

    Abstract Calcium-activated nonselective (CAN) cation channels are expressed in various excitable and nonexcitable Cells supporting important Cellular responses such as neuronal bursting activity, fluid secretion, and cardiac rhythmicity. We have cloned and characterized a second form of TRPM4, TRPM4b, a member of the TRP channel family, as a molecular candidate of a CAN channel. TRPM4b encodes a cation channel of 25 pS unitary conductance that is directly activated by [Ca 2+ ]i with an apparent K D of ∼400 nM. It conducts monovalent cations such as Na + and K + without significant permeation of Ca 2+ . TRPM4b is activated following receptor-mediated Ca 2+ mobilization, representing a regulatory mechanism that controls the magnitude of Ca 2+ influx by modulating the Membrane potential and, with it, the driving force for Ca 2+ entry through other Ca 2+ -permeable pathways.

Ravi F Saraf - One of the best experts on this subject based on the ideXlab platform.

  • noninvasive measurement of electrical events associated with a single chlorovirus infection of a microalgal Cell
    ACS Nano, 2016
    Co-Authors: Gerhard Thiel, Seung Woo Lee, Eun Hee Lee, Ravi F Saraf
    Abstract:

    Chlorovirus Paramecium bursaria chlorella virus 1 (PBCV-1) contains a viral-encoded K+ channel imbedded in its internal Membrane, which triggers host plasma Membrane Depolarization during virus infection. This early stage of infection was monitored at high resolution by recording the Cell Membrane Depolarization of a single Chlorella Cell during infection by a single PBCV-1 particle. The measurement was achieved by depositing the Cells onto a network of one-dimensional necklaces of Au nanoparticles, which spanned two electrodes 70 μm apart. The nanoparticle necklace array has been shown to behave as a single-electron device at room temperature. The resulting electrochemical field-effect transistor (eFET) was gated by the Cell Membrane potential, which allowed a quantitative measurement of the electrophysiological changes across the rigid Cell wall of the microalgae due to a single viral attack at high sensitivity. The single viral infection signature was quantitatively confirmed by coupling the eFET measu...

  • Noninvasive Measurement of Electrical Events Associated with a Single Chlorovirus Infection of a Microalgal Cell
    2016
    Co-Authors: Seung Woo Lee, Gerhard Thiel, Eun Hee Lee, James L. Van Etten, Ravi F Saraf
    Abstract:

    Chlorovirus Paramecium bursaria chlorella virus 1 (PBCV-1) contains a viral-encoded K+ channel imbedded in its internal Membrane, which triggers host plasma Membrane Depolarization during virus infection. This early stage of infection was monitored at high resolution by recording the Cell Membrane Depolarization of a single Chlorella Cell during infection by a single PBCV-1 particle. The measurement was achieved by depositing the Cells onto a network of one-dimensional necklaces of Au nanoparticles, which spanned two electrodes 70 μm apart. The nanoparticle necklace array has been shown to behave as a single-electron device at room temperature. The resulting electrochemical field-effect transistor (eFET) was gated by the Cell Membrane potential, which allowed a quantitative measurement of the electrophysiological changes across the rigid Cell wall of the microalgae due to a single viral attack at high sensitivity. The single viral infection signature was quantitatively confirmed by coupling the eFET measurement with a method in which a single viral particle was delivered for infection by a scanning probe microscope cantilever