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      Endogenous Cardiac Troponin T Modulates Ca 2+-Mediated Smooth Muscle Contraction

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          Abstract

          Mechanisms linked to actin filaments have long been thought to cooperate in smooth muscle contraction, although key molecules were unclear. We show evidence that cardiac troponin T (cTnT) substantially contributes to Ca 2+-mediated contraction in a physiological range of cytosolic Ca 2+ concentration ([Ca 2+] i). cTnT was detected in various smooth muscles of the aorta, trachea, gut and urinary bladder, including in humans. Also, cTnT was distributed along with tropomyosin in smooth muscle cells, suggesting that these proteins are ready to cause smooth muscle contraction. In chemically permeabilised smooth muscle of cTnT +/− mice in which cTnT reduced to ~50%, the Ca 2+-force relationship was shifted toward greater [Ca 2+] i, indicating a sizeable contribution of cTnT to smooth muscle contraction at [Ca 2+] i < 1 μM. Furthermore, addition of supplemental TnI and TnC reconstructed a troponin system to enhance contraction. The results indicated that a Tn/Tn-like system on actin-filaments cooperates together with the thick-filament pathway.

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          Most cited references 32

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          Calcium movements, distribution, and functions in smooth muscle.

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            Smooth muscle signalling pathways in health and disease

            Smooth muscle contractile activity is a major regulator of function of the vascular system, respiratory system, gastrointestinal system and the genitourinary systems. Malfunction of contractility in these systems leads to a host of clinical disorders, and yet, we still have major gaps in our understanding of the molecular mechanisms by which contractility of the differentiated smooth muscle cell is regulated. This review will summarize recent advances in the molecular understanding of the regulation of smooth muscle myosin activity via phosphorylation/dephosphorylation of myosin, the regulation of the accessibility of actin to myosin via the actin-binding proteins calponin and caldesmon, and the remodelling of the actin cytoskeleton. Understanding of the molecular ‘players’ should identify target molecules that could point the way to novel drug discovery programs for the treatment of smooth muscle disorders such as cardiovascular disease, asthma, functional bowel disease and pre-term labour.
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              Calcium ion and muscle contraction.

               S Ebashi,  M. Endo (1967)
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                Author and article information

                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group
                2045-2322
                14 December 2012
                2012
                : 2
                Affiliations
                [1 ]Department of Urology, Kyushu University , Japan
                [2 ]Department of Clinical Pharmacology, Kyushu University , Japan
                [3 ]Department of Pathology, Kyushu University , Japan
                [4 ]Operating Unit for Clinical Trials of Gene Therapy, Graduate School of Medical Sciences, Kyushu University, Japan
                [5 ]Laboratory of Molecular & Cellular Biochemistry, Faculty of Dental Science, Kyushu University , Japan
                [6 ]Special Patient Oral Care Unit, Kyushu University Hospital Fukuoka 812-8582 , Japan
                [7 ]Department of Biomedical Sciences, College of Life and Health Sciences, Chubu University , Kasugai Aichi, 487-8501, Japan
                [8 ]Department of Cell Physiology, Nagoya University Graduate School of Medicine , Nagoya 466-8550, Japan
                Author notes
                Article
                srep00979
                10.1038/srep00979
                3522072
                23248744
                Copyright © 2012, Macmillan Publishers Limited. All rights reserved

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

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