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Transmembrane and Intracellular Translocation of Activator Ca Ions in Cardiac...
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Transmembrane and Intracellular Translocation of Activator Ca Ions in Cardiac and Smooth Muscle Cells

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 6156

Special Issue Editors

Prof. Dr. Suzanne F. Scarlata

E-Mail Website
Guest Editor
Worcester Polytechnic Institute, Worcester, MA, USA
Interests: cell behavior; calcium signals; membrane-associated proteins; membrane properties; G protein signaling
Special Issues, Collections and Topics in MDPI journals
Dr. Haruo Sugi

E-Mail Website
Co-Guest Editor
Department of Physiology, Teikyo University School of Medicine, Tokyo 173-8605, Japan
Interests: physiology and biochemistry of skeletal; cardiac and smooth muscle myosins in health and in disease; compartive aspects of physiology and biochemistry of muscle and mechanism of locomotion; primitive; role of myosins in primitive motile systems; such as amoevoid movement; contractile ring formation; and other cellulr motile functions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It has been well established that muscle contraction results from the elevation of free Ca ion concentration in the interior of muscle cells [Ca2+]i. The Ca2+ producing contraction is called the activator Ca ion.

In cardiac muscle cells, it is generally believed that activator Ca comes from the extracellular fluid in the form of an inward Ca current across the surface membrane, and it is regulated by the Na–Ca exchange mechanism. It has been shown, however, that activator Ca also comes from internal Ca accumulation structures, as indicated by so-called Ca-sparks and recorded by Ca-indicators in relaxed cardiac muscle cells.

In various smooth muscle cells, on the other hand, it has been shown microscopically that activator Ca is stored in internal membrane structures.

This Special Issue on “Transmembrane and Intracellular Translocation of Activator Ca Ions in Cardiac and Smooth Muscle Cells” aims to gather papers addressing the abovementioned topics.

Prof. Dr. Suzanne F. Scarlata
Guest Editor
Dr. Haruo Sugi
Co-Guest Editor

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Published Papers (2 papers)

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Research

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27 pages, 2756 KiB  
Article
Dissecting Cellular Mechanisms of Long-Chain Acylcarnitines-Driven Cardiotoxicity: Disturbance of Calcium Homeostasis, Activation of Ca2+-Dependent Phospholipases, and Mitochondrial Energetics Collapse
by Alexey V. Berezhnov, Evgeniya I. Fedotova, Miroslav N. Nenov, Vitaly A. Kasymov, Oleg Yu. Pimenov and Vladimir V. Dynnik
Int. J. Mol. Sci. 2020, 21(20), 7461; https://doi.org/10.3390/ijms21207461 - 10 Oct 2020
Cited by 18 | Viewed by 3194
Abstract
Long-chain acylcarnitines (LCAC) are implicated in ischemia-reperfusion (I/R)-induced myocardial injury and mitochondrial dysfunction. Yet, molecular mechanisms underlying involvement of LCAC in cardiac injury are not sufficiently studied. It is known that in cardiomyocytes, palmitoylcarnitine (PC) can induce cytosolic Ca2+ accumulation, implicating L-type [...] Read more.
Long-chain acylcarnitines (LCAC) are implicated in ischemia-reperfusion (I/R)-induced myocardial injury and mitochondrial dysfunction. Yet, molecular mechanisms underlying involvement of LCAC in cardiac injury are not sufficiently studied. It is known that in cardiomyocytes, palmitoylcarnitine (PC) can induce cytosolic Ca2+ accumulation, implicating L-type calcium channels, Na+/Ca2+ exchanger, and Ca2+-release from sarcoplasmic reticulum (SR). Alternatively, PC can evoke dissipation of mitochondrial potential (ΔΨm) and mitochondrial permeability transition pore (mPTP). Here, to dissect the complex nature of PC action on Ca2+ homeostasis and oxidative phosphorylation (OXPHOS) in cardiomyocytes and mitochondria, the methods of fluorescent microscopy, perforated path-clamp, and mitochondrial assays were used. We found that LCAC in dose-dependent manner can evoke Ca2+-sparks and oscillations, long-living Ca2+ enriched microdomains, and, finally, Ca2+ overload leading to hypercontracture and cardiomyocyte death. Collectively, PC-driven cardiotoxicity involves: (I) redistribution of Ca2+ from SR to mitochondria with minimal contribution of external calcium influx; (II) irreversible inhibition of Krebs cycle and OXPHOS underlying limited mitochondrial Ca2+ buffering; (III) induction of mPTP reinforced by PC-calcium interplay; (IV) activation of Ca2+-dependent phospholipases cPLA2 and PLC. Based on the inhibitory analysis we may suggest that simultaneous inhibition of both phospholipases could be an effective strategy for protection against PC-mediated toxicity in cardiomyocytes. Full article
(This article belongs to the Special Issue Transmembrane and Intracellular Translocation of Activator Ca Ions in Cardiac and Smooth Muscle Cells)
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Review

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13 pages, 2763 KiB  
Review
Mechanism and Function of the Catch State in Molluscan Smooth Muscle: A Historical Perspective
by Haruo Sugi, Tetsuo Ohno and Masamichi Moriya
Int. J. Mol. Sci. 2020, 21(20), 7576; https://doi.org/10.3390/ijms21207576 - 14 Oct 2020
Cited by 4 | Viewed by 2375
Abstract
Molluscan smooth muscles exhibit the catch state, in which both tension and resistance to stretch are maintained with very low rates of energy consumption. The catch state is studied mainly on the anterior byssus retractor muscle (ABRM) of a bivalve molluscan animal, Mytilus, [...] Read more.
Molluscan smooth muscles exhibit the catch state, in which both tension and resistance to stretch are maintained with very low rates of energy consumption. The catch state is studied mainly on the anterior byssus retractor muscle (ABRM) of a bivalve molluscan animal, Mytilus, which can easily be split into small bundles consisting of parallel fibers. The ABRM contracts actively with an increase in the intracellular free Ca ion concentration, [Ca2+]i, as with all other types of muscle. Meanwhile, the catch state is established after the reduction of [Ca2+]i to the resting level. Despite extensive studies, the mechanism underlying the catch state is not yet fully understood. This article briefly deals with (1) anatomical and ultrastructural aspects of the ABRM, (2) mechanical studies on the transition from the active to the catch state in the isotonic condition, (3) electron microscopic and histochemical studies on the intracellular translocation of Ca ions during the transition from the active to the catch state, and (4) biochemical studies on the catch state, with special reference to a high molecular mass protein, twitchin, which is known to occur in molluscan catch muscles. Full article
(This article belongs to the Special Issue Transmembrane and Intracellular Translocation of Activator Ca Ions in Cardiac and Smooth Muscle Cells)
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