scholarly journals The Role of Membrane Capacitance in Cardiac Impulse Conduction: An Optogenetic Study With Non-excitable Cells Coupled to Cardiomyocytes

2020 ◽  
Vol 11 ◽  
Author(s):  
Stefano Andrea De Simone ◽  
Sarah Moyle ◽  
Andrea Buccarello ◽  
Christian Dellenbach ◽  
Jan Pavel Kucera ◽  
...  
Keyword(s):  
Membrane Capacitance ◽  
Excitable Cells ◽  
Impulse Conduction ◽  
Cardiac Impulse

scholarly journals Association of Interatrial Septal Abnormalities with Cardiac Impulse Conduction Disorders in Adult Patients: Experience from a Tertiary Center in Kosovo

2011 ◽  
Vol 6 (1) ◽  
pp. hi.2011.e4 ◽  
Author(s):  
Aurora Bakalli ◽  
Ejup Pllana ◽  
Dardan Koçinaj ◽  
Tefik Bekteshi ◽  
Gani Dragusha ◽  
...  
Keyword(s):  
Adult Patients ◽  
Impulse Conduction ◽  
Conduction Disorders ◽  
Cardiac Impulse ◽  
Tertiary Center ◽  
Patients Experience

scholarly journals Cardiac macrophages prevent sudden death during heart stress

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Junichi Sugita ◽  
Katsuhito Fujiu ◽  
Yukiteru Nakayama ◽  
Takumi Matsubara ◽  
Jun Matsuda ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Sudden Death ◽  
Gap Junctions ◽  
Adrenergic Receptor ◽  
Cardiac Death ◽  
Connexin 43 ◽  
Pressure Overload ◽  
Impulse Conduction ◽  
Cardiac Impulse ◽  
Medical Need

AbstractCardiac arrhythmias are a primary contributor to sudden cardiac death, a major unmet medical need. Because right ventricular (RV) dysfunction increases the risk for sudden cardiac death, we examined responses to RV stress in mice. Among immune cells accumulated in the RV after pressure overload-induced by pulmonary artery banding, interfering with macrophages caused sudden death from severe arrhythmias. We show that cardiac macrophages crucially maintain cardiac impulse conduction by facilitating myocardial intercellular communication through gap junctions. Amphiregulin (AREG) produced by cardiac macrophages is a key mediator that controls connexin 43 phosphorylation and translocation in cardiomyocytes. Deletion of Areg from macrophages led to disorganization of gap junctions and, in turn, lethal arrhythmias during acute stresses, including RV pressure overload and β-adrenergic receptor stimulation. These results suggest that AREG from cardiac resident macrophages is a critical regulator of cardiac impulse conduction and may be a useful therapeutic target for the prevention of sudden death.

scholarly journals Calnexin revealed as an ether-a-go-go chaperone by getting mutant worms up and going

2018 ◽  
Vol 150 (8) ◽  
pp. 1059-1061
Author(s):  
Jonathan T. Pierce
Keyword(s):  
Ion Channels ◽  
Dynamic Control ◽  
Cell Types ◽  
K Channel ◽  
Membrane Domains ◽  
Excitable Cells ◽  
Patch Clamp Recording ◽  
Cell Excitability ◽  
Distinct Membrane

The role of ion channels in cell excitability was first revealed in a series of voltage clamp experiments by Hodgkin and Huxley in the 1950s. However, it was not until the 1970s that patch-clamp recording ushered in a revolution that allowed physiologists to witness how ion channels flicker open and closed at angstrom scale and with microsecond resolution. The unexpectedly tight seal made by the patch pipette in the whole-cell configuration later allowed molecular biologists to suck up the insides of identified cells to unveil their unique molecular contents. By refining these techniques, researchers have scrutinized the surface and contents of excitable cells in detail over the past few decades. However, these powerful approaches do not discern which molecules are responsible for the dynamic control of the genesis, abundance, and subcellular localization of ion channels. In this dark territory, teams of unknown and poorly understood molecules guide specific ion channels through translation, folding, and modification, and then they shuttle them toward and away from distinct membrane domains via different subcellular routes. A central challenge in understanding these processes is the likelihood that these diverse regulatory molecules may be specific to ion channel subtypes, cell types, and circumstance. In work described in this issue, Bai et al. (2018. J. Gen. Physiol. https://doi.org/10.1085/jgp.201812025) begin to shed light on the biogenesis of UNC-103, a K+ channel found in Caenorhabditis elegans.

scholarly journals Silencing of Plasma Membrane Ca2+-ATPase Isoforms 2 and 3 Impairs Energy Metabolism in Differentiating PC12 Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Tomasz Boczek ◽  
Malwina Lisek ◽  
Bozena Ferenc ◽  
Antoni Kowalski ◽  
Magdalena Wiktorska ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Pc12 Cells ◽  
Molecular Mechanisms ◽  
Atp Synthesis ◽  
Mitochondrial Activity ◽  
Excitable Cells ◽  
Close Link ◽  
Atp Level ◽  
Atp Generation

A close link between Ca2+, ATP level, and neurogenesis is apparent; however, the molecular mechanisms of this relationship have not been completely elucidated. Transient elevations of cytosolic Ca2+may boost ATP synthesis, but ATP is also consumed by ion pumps to maintain a low Ca2+in cytosol. In differentiation process plasma membrane Ca2+ATPase (PMCA) is considered as one of the major players for Ca2+homeostasis. From four PMCA isoforms, the fastest PMCA2 and PMCA3 are expressed predominantly in excitable cells. In the present study we assessed whether PMCA isoform composition may affect energy balance in differentiating PC12 cells. We found that PMCA2-downregulated cells showed higher basal O2consumption, lower NAD(P)H level, and increased activity of ETC. These changes associated with higher[Ca2+]cresulted in elevated ATP level. Since PMCA2-reduced cells demonstrated greatest sensitivity to ETC inhibition, we suppose that the main source of energy for PMCA isoforms 1, 3, and 4 was oxidative phosphorylation. Contrary, cells with unchanged PMCA2 expression exhibited prevalence of glycolysis in ATP generation. Our results with PMCA2- or PMCA3-downregulated lines provide an evidence of a novel role of PMCA isoforms in regulation of bioenergetic pathways, and mitochondrial activity and maintenance of ATP level during PC12 cells differentiation.

scholarly journals Inositol 1,4,5-Trisphosphate Directs Ca2+Flow between Mitochondria and the Endoplasmic/Sarcoplasmic Reticulum: A Role in Regulating Cardiac Autonomic Ca2+ Spiking

2000 ◽  
Vol 11 (5) ◽  
pp. 1845-1858 ◽  
Author(s):  
Marisa Jaconi ◽  
Claire Bony ◽  
Stephen M. Richards ◽  
André Terzic ◽  
Serge Arnaudeau ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Dominant Negative ◽  
Neonatal Rat ◽  
Excitable Cells ◽  
Rat Cardiomyocytes ◽  
Cell Functions ◽  
Inositol 1,4,5 Trisphosphate ◽  
Cellular Ca ◽  
Cardiac Autonomic Activity

The signaling role of the Ca2+ releaser inositol 1,4,5-trisphosphate (IP3) has been associated with diverse cell functions. Yet, the physiological significance of IP3 in tissues that feature a ryanodine-sensitive sarcoplasmic reticulum has remained elusive. IP3 generated by photolysis of caged IP3 or by purinergic activation of phospholipase Cγ slowed down or abolished autonomic Ca2+ spiking in neonatal rat cardiomyocytes. Microinjection of heparin, blocking dominant-negative fusion protein, or anti-phospholipase Cγ antibody prevented the IP3-mediated purinergic effect. IP3 triggered a ryanodine- and caffeine-insensitive Ca2+ release restricted to the perinuclear region. In cells loaded with Rhod2 or expressing a mitochondria-targeted cameleon and TMRM to monitor mitochondrial Ca2+ and potential, IP3 induced transient Ca2+ loading and depolarization of the organelles. These mitochondrial changes were associated with Ca2+ depletion of the sarcoplasmic reticulum and preceded the arrest of cellular Ca2+ spiking. Thus, IP3 acting within a restricted cellular region regulates the dynamic of calcium flow between mitochondria and the endoplasmic/sarcoplasmic reticulum. We have thus uncovered a novel role for IP3 in excitable cells, the regulation of cardiac autonomic activity.

scholarly journals A triggered mechanism retrieves membrane in seconds after Ca(2+)-stimulated exocytosis in single pituitary cells

1994 ◽  
Vol 124 (5) ◽  
pp. 667-675 ◽  
Author(s):  
P Thomas ◽  
AK Lee ◽  
JG Wong ◽  
W Almers
Keyword(s):  
Plasma Membrane ◽  
Cell Surface ◽  
Time Constant ◽  
Flash Photolysis ◽  
Membrane Capacitance ◽  
Coated Vesicles ◽  
Neuroendocrine Cells ◽  
Pituitary Cells ◽  
Excitable Cells ◽  
Late Step

In neuroendocrine cells, cytosolic Ca2+ triggers exocytosis in tens of milliseconds, yet known pathways of endocytic membrane retrieval take minutes. To test for faster retrieval mechanisms, we have triggered short bursts of exocytosis by flash photolysis of caged Ca2+, and have tracked subsequent retrieval by measuring the plasma membrane capacitance. We find that a limited amount of membrane can be retrieved with a time constant of 4 s at 21-26 degrees C, and that this occurs partially via structures larger than coated vesicles. This novel mechanism may be arrested at a late step. Incomplete retrieval structures then remain on the cell surface for minutes until the consequences of a renewed increase in cytosolic [Ca2+] disconnect them from the cell surface in < 1 s. Our results provide evidence for a rapid, triggered membrane retrieval pathway in excitable cells.

scholarly journals TASK-1 (KCNK3) channels in the lung: from cell biology to clinical implications

2017 ◽  
Vol 50 (5) ◽  
pp. 1700754 ◽  
Author(s):  
Andrea Olschewski ◽  
Emma L. Veale ◽  
Bence M. Nagy ◽  
Chandran Nagaraj ◽  
Grazyna Kwapiszewska ◽  
...  
Keyword(s):  
Pulmonary Circulation ◽  
Cell Biology ◽  
Unsaturated Fatty Acids ◽  
Excitable Cells ◽  
Intracellular Signalling Pathways ◽  
Current State ◽  
Health And Disease ◽  
Pulmonary Arterial ◽  
Pore Domain

TWIK-related acid-sensitive potassium channel 1 (TASK-1 encoded by KCNK3) belongs to the family of two-pore domain potassium channels. This gene subfamily is constitutively active at physiological resting membrane potentials in excitable cells, including smooth muscle cells, and has been particularly linked to the human pulmonary circulation. TASK-1 channels are sensitive to a wide array of physiological and pharmacological mediators that affect their activity such as unsaturated fatty acids, extracellular pH, hypoxia, anaesthetics and intracellular signalling pathways. Recent studies show that modulation of TASK-1 channels, either directly or indirectly by targeting their regulatory mechanisms, has the potential to control pulmonary arterial tone in humans. Furthermore, mutations in KCNK3 have been identified as a rare cause of both familial and idiopathic pulmonary arterial hypertension. This review summarises our current state of knowledge of the functional role of TASK-1 channels in the pulmonary circulation in health and disease, with special emphasis on current advancements in the field.

scholarly journals Role of STIM1 protein in the regulation of store-operated channels in non-excitable cells

2009 ◽  
Vol 3 (3) ◽  
pp. 329-329
Author(s):  
I. A. Pozdnjakov ◽  
V. A. Vigont ◽  
O. A. Zimina ◽  
A. Yu. Skopin ◽  
L. N. Glushankova ◽  
...  
Keyword(s):  
Excitable Cells
Sign in / Sign up

Export Citation Format

Share Document