Studies on Slow Cardiac Action Potentials Occurring in Potassium-Rich Media as a Simulation of the Early Phase of Myocardial Infarction

1983 ◽  
pp. 589-594 ◽  
Author(s):  
M. Sebeszta ◽  
E. Coraboeuf
Keyword(s):  
Myocardial Infarction ◽  
Early Phase ◽  
Action Potentials ◽  
Cardiac Action ◽  
Rich Media

New Molecular Scaffolds for Fluorescent Voltage Indicators

2018 ◽  
Author(s):  
Steven Boggess ◽  
Shivaani Gandhi ◽  
Brian Siemons ◽  
Nathaniel Huebsch ◽  
Kevin Healy ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Induced Pluripotent Stem Cell ◽  
Molecular Wire ◽  
Voltage Sensing ◽  
Design Synthesis ◽  
Cardiac Action ◽  
Action Potential Waveform ◽  
Induced Pluripotent ◽  
Voltage Sensing Domain

<div> <p>The ability to non-invasively monitor membrane potential dynamics in excitable cells like neurons and cardiomyocytes promises to revolutionize our understanding of the physiology and pathology of the brain and heart. Here, we report the design, synthesis, and application of a new class of fluorescent voltage indicator that makes use of a fluorene-based molecular wire as a voltage sensing domain to provide fast and sensitive measurements of membrane potential in both mammalian neurons and human-derived cardiomyocytes. We show that the best of the new probes, fluorene VoltageFluor 2 (fVF 2) readily reports on action potentials in mammalian neurons, detects perturbations to cardiac action potential waveform in human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes, shows a substantial decrease in phototoxicity compared to existing molecular wire-based indicators, and can monitor cardiac action potentials for extended periods of time. Together, our results demonstrate the generalizability of a molecular wire approach to voltage sensing and highlights the utility of fVF 2 for interrogating membrane potential dynamics.</p> </div>

Nucleolin Improves Heart Function During Recovery From Myocardial Infarction by Modulating Macrophage Polarization

2021 ◽  
pp. 107424842198957
Author(s):  
Yuting Tang ◽  
Xiaofang Lin ◽  
Cheng Chen ◽  
Zhongyi Tong ◽  
Hui Sun ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Early Phase ◽  
Heart Function ◽  
Macrophage Polarization ◽  
Late Phase ◽  
Macrophage Infiltration ◽  
Enzyme Linked Immunosorbent Assay ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization ◽  
Nucleolin Expression

Background: Nucleolin has multiple functions within cell survival and proliferation pathways. Our previous studies have revealed that nucleolin can significantly reduce myocardial ischemia-reperfusion injury by promoting myocardial angiogenesis and reducing myocardial apoptosis. In this study, we attempted to determine the role of nucleolin in myocardial infarction (MI) injury recovery and the underlying mechanism. Methods: Male BALB/c mice aged 6–8 weeks were used to set up MI models by ligating the left anterior descending coronary artery. Nucleolin expression in the heart was downregulated by intramyocardial injection of a lentiviral vector expressing nucleolin-specific small interfering RNA. Macrophage infiltration and polarization were measured by real-time polymerase chain reaction, flow cytometry, and immunofluorescence. Cytokines were detected by enzyme-linked immunosorbent assay. Results: Nucleolin expression in myocardium after MI induction decreased a lot at early phase and elevated at late phase. Nucleolin knockdown impaired heart systolic and diastolic functions and decreased the survival rate after MI. Macrophage infiltration increased in the myocardium after MI. Most macrophages belonged to the M1 phenotype at early phase (2 days) and the M2 phenotype increased greatly at late phase after MI. Nucleolin knockdown in the myocardium led to a decrease in M2 macrophage polarization with no effect on macrophage infiltration after MI. Furthermore, Notch3 and STAT6, key regulators of M2 macrophage polarization, were upregulated by nucleolin in RAW 264.7 macrophages. Conclusions: Lack of nucleolin impaired heart function during recovery after MI by reducing M2 macrophage polarization. This finding probably points to a new therapeutic option for ischemic heart disease.

The long-lasting cardiac action potentials are related to pressure generation in the heart

2021 ◽  
Author(s):  
José Guilherme Chaui-Berlinck ◽  
Vitor Rodrigues da Silva
Keyword(s):  
Action Potentials ◽  
Cardiac Action

scholarly journals Roles of Cyclooxygenase 2 in Sevoflurane- and Olprinone-Induced Early Phase of Preconditioning and Postconditioning Against Myocardial Infarction in Rat Hearts

2010 ◽  
Vol 16 (1) ◽  
pp. 72-78 ◽  
Author(s):  
Shinya Tosaka ◽  
Reiko Tosaka ◽  
Shuhei Matsumoto ◽  
Takuji Maekawa ◽  
Sungsam Cho ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Early Phase ◽  
Cyclooxygenase 2 ◽  
Rat Hearts

The influence of fibroblast co-culture and 3D structures on cardiac action potentials of human stem cell-derived cardiomyocytes

2018 ◽  
Vol 93 ◽  
pp. 169
Author(s):  
Maria P. Hortigon-Vinagre ◽  
Victor Zamora ◽  
Gary Gintant ◽  
Jonathon Green ◽  
Francis L. Burton ◽  
...  
Keyword(s):  
Stem Cell ◽  
Action Potentials ◽  
Human Stem Cell ◽  
3D Structures ◽  
Cardiac Action

scholarly journals KCNE1 and KCNE3 modulate KCNQ1 channels by affecting different gating transitions

2017 ◽  
Vol 114 (35) ◽  
pp. E7367-E7376 ◽  
Author(s):  
Rene Barro-Soria ◽  
Rosamary Ramentol ◽  
Sara I. Liin ◽  
Marta E. Perez ◽  
Robert S. Kass ◽  
...  
Keyword(s):  
Action Potentials ◽  
Potassium Current ◽  
Voltage Sensor ◽  
Α Subunit ◽  
Voltage Range ◽  
Gate Opening ◽  
Cardiac Action ◽  
Repolarization Phase ◽  
Voltage Dependent ◽  
Salt Secretion

KCNE β-subunits assemble with and modulate the properties of voltage-gated K+ channels. In the heart, KCNE1 associates with the α-subunit KCNQ1 to generate the slowly activating, voltage-dependent potassium current (IKs) in the heart that controls the repolarization phase of cardiac action potentials. By contrast, in epithelial cells from the colon, stomach, and kidney, KCNE3 coassembles with KCNQ1 to form K+ channels that are voltage-independent K+ channels in the physiological voltage range and important for controlling water and salt secretion and absorption. How KCNE1 and KCNE3 subunits modify KCNQ1 channel gating so differently is largely unknown. Here, we use voltage clamp fluorometry to determine how KCNE1 and KCNE3 affect the voltage sensor and the gate of KCNQ1. By separating S4 movement and gate opening by mutations or phosphatidylinositol 4,5-bisphosphate depletion, we show that KCNE1 affects both the S4 movement and the gate, whereas KCNE3 affects the S4 movement and only affects the gate in KCNQ1 if an intact S4-to-gate coupling is present. Further, we show that a triple mutation in the middle of the transmembrane (TM) segment of KCNE3 introduces KCNE1-like effects on the second S4 movement and the gate. In addition, we show that differences in two residues at the external end of the KCNE TM segments underlie differences in the effects of the different KCNEs on the first S4 movement and the voltage sensor-to-gate coupling.

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