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Dr. Haruo Sugi
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Department of Physiology, Teikyo University, Itabashi-ku, Tokyo, 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
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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.

Dr. Haruo Sugi
Guest Editor

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Open AccessArticle

Dissecting Cellular Mechanisms of Long-Chain Acylcarnitines-Driven Cardiotoxicity: Disturbance of Calcium Homeostasis, Activation of Ca²⁺-Dependent Phospholipases, and Mitochondrial Energetics Collapse

and

Int. J. Mol. Sci. 2020, 21(20), 7461; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21207461 - 10 Oct 2020

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 calcium channels, Na⁺/Ca²⁺ exchanger, and Ca²⁺-release from sarcoplasmic reticulum (SR). Alternatively, PC can evoke dissipation of mitochondrial potential (ΔΨ_m) 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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Open AccessReview

Mechanism and Function of the Catch State in Molluscan Smooth Muscle: A Historical Perspective

Haruo Sugi

Tetsuo Ohno

and

Masamichi Moriya

Int. J. Mol. Sci. 2020, 21(20), 7576; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21207576 - 14 Oct 2020

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, 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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