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  1. AU="Ruben, Peter C"
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  1. Book: Voltage gated sodium channels

    Ruben, Peter C.

    (Handbook of experimental pharmacology ; 221)

    2014  

    Author's details Peter C. Ruben ed
    Series title Handbook of experimental pharmacology ; 221
    Collection
    Keywords Natriumkanal ; Spannungskontrollierter Ionenkanal ; Pathophysiologie ; Erbkrankheit
    Subject Spannungsaktivierter Ionenkanal ; Spannungsgesteuerter Ionenkanal ; Genetische Krankheit ; Heredopathie ; Genetisch bedingte Krankheit ; Genetisches Syndrom ; Erbkrankheiten ; Pathologische Physiologie ; Physiologische Pathologie ; Physiopathologie
    Language English
    Size VIII, 295 S. :Ill., graph. Darst., 235 mm x 155 mm
    Publisher Springer
    Publishing place Heidelberg u.a.
    Publishing country Germany
    Document type Book
    HBZ-ID HT018252795
    ISBN 978-3-642-41587-6 ; 3-642-41587-3
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2014 A 1892 available for loan (reading room) Lesesaal EG

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  2. Article ; Online: Cannabidiol potentiates hyperpolarization-activated cyclic nucleotide-gated (HCN4) channels.

    Page, Dana A / Ruben, Peter C

    The Journal of general physiology

    2024  Volume 156, Issue 6

    Abstract: Cannabidiol (CBD), the main non-psychotropic phytocannabinoid produced by the Cannabis sativa plant, blocks a variety of cardiac ion channels. We aimed to identify whether CBD regulated the cardiac pacemaker channel or the hyperpolarization-activated ... ...

    Abstract Cannabidiol (CBD), the main non-psychotropic phytocannabinoid produced by the Cannabis sativa plant, blocks a variety of cardiac ion channels. We aimed to identify whether CBD regulated the cardiac pacemaker channel or the hyperpolarization-activated cyclic nucleotide-gated channel (HCN4). HCN4 channels are important for the generation of the action potential in the sinoatrial node of the heart and increased heart rate in response to β-adrenergic stimulation. HCN4 channels were expressed in HEK 293T cells, and the effect of CBD application was examined using a whole-cell patch clamp. We found that CBD depolarized the V1/2 of activation in holo-HCN4 channels, with an EC50 of 1.6 µM, without changing the current density. CBD also sped activation kinetics by approximately threefold. CBD potentiation of HCN4 channels occurred via binding to the closed state of the channel. We found that CBD's mechanism of action was distinct from cAMP, as CBD also potentiated apo-HCN4 channels. The addition of an exogenous PIP2 analog did not alter the ability of CBD to potentiate HCN4 channels, suggesting that CBD also acts using a unique mechanism from the known HCN4 potentiator PIP2. Lastly, to gain insight into CBD's mechanism of action, computational modeling and targeted mutagenesis were used to predict that CBD binds to a lipid-binding pocket at the C-terminus of the voltage sensor. CBD represents the first FDA-approved drug to potentiate HCN4 channels, and our findings suggest a novel starting point for drug development targeting HCN4 channels.
    MeSH term(s) Cannabidiol/pharmacology ; Humans ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels/metabolism ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels/genetics ; HEK293 Cells ; Potassium Channels/metabolism ; Potassium Channels/drug effects ; Ion Channel Gating/drug effects ; Muscle Proteins
    Chemical Substances Cannabidiol (19GBJ60SN5) ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels ; HCN4 protein, human ; Potassium Channels ; Muscle Proteins
    Language English
    Publishing date 2024-04-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 3118-5
    ISSN 1540-7748 ; 0022-1295
    ISSN (online) 1540-7748
    ISSN 0022-1295
    DOI 10.1085/jgp.202313505
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Editorial: Cannabinoid interactions with ion channels, receptors, and the bio-membrane.

    Ghovanloo, Mohammad-Reza / Arnold, Jonathon C / Ruben, Peter C

    Frontiers in physiology

    2023  Volume 14, Page(s) 1211230

    Language English
    Publishing date 2023-05-09
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2023.1211230
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Protein Kinases Mediate Anti-Inflammatory Effects of Cannabidiol and Estradiol Against High Glucose in Cardiac Sodium Channels.

    Fouda, Mohamed A / Ruben, Peter C

    Frontiers in pharmacology

    2021  Volume 12, Page(s) 668657

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2021-04-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2021.668657
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Cannabidiol and Sodium Channel Pharmacology: General Overview, Mechanism, and Clinical Implications.

    Ghovanloo, Mohammad-Reza / Ruben, Peter C

    The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry

    2021  Volume 28, Issue 4, Page(s) 318–334

    Abstract: Voltage-gated sodium (Nav) channels initiate action potentials in excitable tissues. Altering these channels' function can lead to many pathophysiological conditions. Nav channels are composed of several functional and structural domains that could be ... ...

    Abstract Voltage-gated sodium (Nav) channels initiate action potentials in excitable tissues. Altering these channels' function can lead to many pathophysiological conditions. Nav channels are composed of several functional and structural domains that could be targeted pharmacologically as potential therapeutic means against various neurological conditions. Mutations in Nav channels have been suggested to underlie various clinical syndromes in different tissues and in association with conditions ranging from epileptic to muscular problems. Treating those mutations that increase the excitability of Nav channels requires inhibitors that could effectively reduce channel firing. The main non-psychotropic constituent of the cannabis plant, cannabidiol (CBD), has recently gained interest as a viable compound to treat some of the conditions that are associated with Nav malfunctions. In this review, we discuss an overview of Nav channels followed by an in-depth description of the interactions of CBD and Nav channels. We conclude with some clinical implications of CBD use against Nav hyperexcitability based on a series of preclinical studies published to date, with a focus on Nav/CBD interactions.
    MeSH term(s) Action Potentials ; Cannabidiol/pharmacology ; Cannabidiol/therapeutic use ; Epilepsy/drug therapy ; Humans ; Voltage-Gated Sodium Channels
    Chemical Substances Voltage-Gated Sodium Channels ; Cannabidiol (19GBJ60SN5)
    Language English
    Publishing date 2021-05-24
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1233753-5
    ISSN 1089-4098 ; 1073-8584
    ISSN (online) 1089-4098
    ISSN 1073-8584
    DOI 10.1177/10738584211017009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4315: Show issues Location:
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  6. Article ; Online: Cannabidiol increases gramicidin current in human embryonic kidney cells: An observational study.

    Ghovanloo, Mohammad-Reza / Goodchild, Samuel J / Ruben, Peter C

    PloS one

    2022  Volume 17, Issue 8, Page(s) e0271801

    Abstract: Gramicidin is a monomeric protein that is thought to non-selectively conduct cationic currents and water. Linear gramicidin is considered an antibiotic. This function is considered to be mediated by the formation of pores within the lipid membrane, ... ...

    Abstract Gramicidin is a monomeric protein that is thought to non-selectively conduct cationic currents and water. Linear gramicidin is considered an antibiotic. This function is considered to be mediated by the formation of pores within the lipid membrane, thereby killing bacterial cells. The main non-psychoactive active constituent of the cannabis plant, cannabidiol (CBD), has recently gained interest, and is proposed to possess various potential therapeutic properties, including being an antibiotic. We previously determined that CBD's activity on ion channels could be, in part, mediated by altering membrane biophysical properties, including elasticity. In this study, our goal was to determine the empirical effects of CBD on gramicidin currents in human embryonic kidney (HEK) cells, seeking to infer potential direct compound-protein interactions. Our results indicate that gramicidin, when applied to the extracellular HEK cell membrane, followed by CBD perfusion, increases the gramicidin current.
    MeSH term(s) Anti-Bacterial Agents/therapeutic use ; Cannabidiol/therapeutic use ; Cannabis/metabolism ; Gramicidin/pharmacology ; Humans ; Kidney/metabolism
    Chemical Substances Anti-Bacterial Agents ; Gramicidin (1405-97-6) ; Cannabidiol (19GBJ60SN5)
    Language English
    Publishing date 2022-08-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0271801
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: ARumenamides

    Abdelsayed, Mena / Page, Dana / Ruben, Peter C

    Frontiers in pharmacology

    2022  Volume 13, Page(s) 976903

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2022-09-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2022.976903
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  8. Article ; Online: Late sodium current: incomplete inactivation triggers seizures, myotonias, arrhythmias, and pain syndromes.

    Fouda, Mohamed A / Ghovanloo, Mohammad-Reza / Ruben, Peter C

    The Journal of physiology

    2022  Volume 600, Issue 12, Page(s) 2835–2851

    Abstract: Acquired and inherited dysfunction in voltage-gated sodium channels underlies a wide range of diseases. In addition to defects in trafficking and expression, sodium channelopathies are caused by dysfunction in one or several gating properties, for ... ...

    Abstract Acquired and inherited dysfunction in voltage-gated sodium channels underlies a wide range of diseases. In addition to defects in trafficking and expression, sodium channelopathies are caused by dysfunction in one or several gating properties, for instance activation or inactivation. Disruption of channel inactivation leads to increased late sodium current, which is a common defect in seizure disorders, cardiac arrhythmias skeletal muscle myotonia and pain. An increase in late sodium current leads to repetitive action potentials in neurons and skeletal muscles, and prolonged action potential duration in the heart. In this Topical Review, we compare the effects of late sodium current in brain, heart, skeletal muscle and peripheral nerves.
    MeSH term(s) Arrhythmias, Cardiac ; Humans ; Myotonia/metabolism ; Pain ; Sodium/metabolism ; Syndrome
    Chemical Substances Sodium (9NEZ333N27)
    Language English
    Publishing date 2022-04-27
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/JP282768
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.65: Show issues Location:
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  9. Article: Say Cheese: Structure of the Cardiac Electrical Engine Is Captured.

    Ghovanloo, Mohammad-Reza / Ruben, Peter C

    Trends in biochemical sciences

    2020  Volume 45, Issue 5, Page(s) 369–371

    Abstract: Voltage-gated sodium channel (Nav)1.5 is the predominantly expressed sodium channel in the myocardium. Mutations in the gene encoding Nav1.5 are associated with several types of cardiac arrhythmias. In their recent study, Jiang et al. provide a detailed ... ...

    Abstract Voltage-gated sodium channel (Nav)1.5 is the predominantly expressed sodium channel in the myocardium. Mutations in the gene encoding Nav1.5 are associated with several types of cardiac arrhythmias. In their recent study, Jiang et al. provide a detailed structure of the rat Nav1.5, with major implications regarding its physiology, pharmacology, and pathophysiology.
    MeSH term(s) Animals ; Cheese ; Mutation ; NAV1.5 Voltage-Gated Sodium Channel/genetics ; Rats
    Chemical Substances NAV1.5 Voltage-Gated Sodium Channel
    Language English
    Publishing date 2020-02-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 194216-5
    ISSN 1362-4326 ; 0968-0004 ; 0376-5067
    ISSN (online) 1362-4326
    ISSN 0968-0004 ; 0376-5067
    DOI 10.1016/j.tibs.2020.02.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1207: Show issues Location:
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  10. Article ; Online: Anti-inflammatory effects of cannabidiol against lipopolysaccharides in cardiac sodium channels.

    Fouda, Mohamed A / Fathy Mohamed, Yasmine / Fernandez, Rachel / Ruben, Peter C

    British journal of pharmacology

    2022  Volume 179, Issue 24, Page(s) 5259–5272

    Abstract: Background: Sepsis, caused by a dysregulated response to infections, can lead to cardiac arrhythmias. However, the mechanisms underlying sepsis-induced inflammation, and how inflammation provokes cardiac arrhythmias, are not well understood. We ... ...

    Abstract Background: Sepsis, caused by a dysregulated response to infections, can lead to cardiac arrhythmias. However, the mechanisms underlying sepsis-induced inflammation, and how inflammation provokes cardiac arrhythmias, are not well understood. We hypothesized that cannabidiol (CBD) may ameliorate lipopolysaccharide (LPS)-induced cardiotoxicity, via Toll-like receptors (TLR4) and cardiac sodium channels (Na<sub>V</sub> 1.5).
    Methods and results: We incubated human immune cells (THP-1 macrophages) with LPS for 24 h, then extracted the THP-1 incubation media. ELISA assays showed that LPS (1 or 5 μg·ml<sup>-1</sup> ), in a concentration-dependent manner, or MPLA (TLR4 agonist, 5 μg·ml<sup>-1</sup> ) stimulated the THP-1 cells to release inflammatory cytokines (TNF-α and IL-6). Prior incubation (4 h) with CBD (5 μM) or C34 (TLR4 antagonist: 5 μg·ml<sup>-1</sup> ) inhibited LPS and MPLA-induced release of both IL-6 and TNF-α. Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM) were subsequently incubated for 24 h in the media extracted from THP-1 cells incubated with LPS, MPLA alone, or in combination with CBD or C34. Voltage-clamp experiments showed a right shift in the voltage dependence of Na<sub>V</sub> 1.5 activation, steady state fast inactivation (SSFI), increased persistent current and prolonged in silico action potential duration in hiSPC-CMs incubated in the LPS or MPLA-THP-1 media. Co-incubation with CBD or C34 rescued the biophysical dysfunction caused by LPS and MPLA.
    Conclusion: Our results suggest that CBD may protect against sepsis-induced inflammation and subsequent arrhythmias through (i) inhibition of the release of inflammatory cytokines, antioxidant and anti-apoptotic effects and/or (ii) a direct effect on Na<sub>V</sub> 1.5.
    MeSH term(s) Humans ; Anti-Inflammatory Agents/pharmacology ; Cannabidiol/pharmacology ; Cytokines/metabolism ; Inflammation ; Interleukin-6 ; Lipopolysaccharides/pharmacology ; Sepsis ; Sodium Channels ; Toll-Like Receptor 4/metabolism ; Tumor Necrosis Factor-alpha
    Chemical Substances Anti-Inflammatory Agents ; Cannabidiol (19GBJ60SN5) ; Cytokines ; Interleukin-6 ; Lipopolysaccharides ; Sodium Channels ; Toll-Like Receptor 4 ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2022-08-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.15936
    Database MEDical Literature Analysis and Retrieval System OnLINE

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