Store-Operated Ca2+ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle

Muscle atrophy alone is insufficient to explain the significant decline in contractile force of skeletal muscle during normal aging. One contributing factor to decreased contractile force in aging skeletal muscle could be compromised excitation-contraction (E-C) coupling, without sufficient availabl...

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Main Authors:	Thornton, Angela M, Zhao, Xiaoli, Weisleder, Noah, Brotto, Leticia S., Bougoin, Sylvain, Nosek, Thomas M., Reid, Michael, Hardin, Brian, Pan, Zui, Ma, Jianjie, Parness, Jerome, Brotto, Marco
Format:	Online
Language:	English
Published:	Impact Journals LLC 2011
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164370/

id	pubmed-3164370
recordtype	oai_dc
spelling	pubmed-31643702011-09-02 Store-Operated Ca2+ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle Thornton, Angela M Zhao, Xiaoli Weisleder, Noah Brotto, Leticia S. Bougoin, Sylvain Nosek, Thomas M. Reid, Michael Hardin, Brian Pan, Zui Ma, Jianjie Parness, Jerome Brotto, Marco Research Paper Muscle atrophy alone is insufficient to explain the significant decline in contractile force of skeletal muscle during normal aging. One contributing factor to decreased contractile force in aging skeletal muscle could be compromised excitation-contraction (E-C) coupling, without sufficient available Ca2+ to allow for repetitive muscle contractility, skeletal muscles naturally become weaker. Using biophysical approaches, we previously showed that store-operated Ca2+ entry (SOCE) is compromised in aged skeletal muscle but not in young ones. While important, a missing component from previous studies is whether or not SOCE function correlates with contractile function during aging. Here we test the contribution of extracellular Ca2+ to contractile function of skeletal muscle during aging. First, we demonstrate graded coupling between SR Ca2+ release channel-mediated Ca2+ release and activation of SOCE. Inhibition of SOCE produced significant reduction of contractile force in young skeletal muscle, particularly at high frequency stimulation, and such effects were completely absent in aged skeletal muscle. Our data indicate that SOCE contributes to the normal physiological contractile response of young healthy skeletal muscle and that defective extracellular Ca2+ entry through SOCE contributes to the reduced contractile force characteristic of aged skeletal muscle. Impact Journals LLC 2011-06-06 /pmc/articles/PMC3164370/ /pubmed/21666285 Text en Copyright: © 2011 Thornton et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Thornton, Angela M Zhao, Xiaoli Weisleder, Noah Brotto, Leticia S. Bougoin, Sylvain Nosek, Thomas M. Reid, Michael Hardin, Brian Pan, Zui Ma, Jianjie Parness, Jerome Brotto, Marco
spellingShingle	Thornton, Angela M Zhao, Xiaoli Weisleder, Noah Brotto, Leticia S. Bougoin, Sylvain Nosek, Thomas M. Reid, Michael Hardin, Brian Pan, Zui Ma, Jianjie Parness, Jerome Brotto, Marco Store-Operated Ca2+ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle
author_facet	Thornton, Angela M Zhao, Xiaoli Weisleder, Noah Brotto, Leticia S. Bougoin, Sylvain Nosek, Thomas M. Reid, Michael Hardin, Brian Pan, Zui Ma, Jianjie Parness, Jerome Brotto, Marco
author_sort	Thornton, Angela M
title	Store-Operated Ca2+ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle
title_short	Store-Operated Ca2+ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle
title_full	Store-Operated Ca2+ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle
title_fullStr	Store-Operated Ca2+ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle
title_full_unstemmed	Store-Operated Ca2+ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle
title_sort	store-operated ca2+ entry (soce) contributes to normal skeletal muscle contractility in young but not in aged skeletal muscle
description	Muscle atrophy alone is insufficient to explain the significant decline in contractile force of skeletal muscle during normal aging. One contributing factor to decreased contractile force in aging skeletal muscle could be compromised excitation-contraction (E-C) coupling, without sufficient available Ca2+ to allow for repetitive muscle contractility, skeletal muscles naturally become weaker. Using biophysical approaches, we previously showed that store-operated Ca2+ entry (SOCE) is compromised in aged skeletal muscle but not in young ones. While important, a missing component from previous studies is whether or not SOCE function correlates with contractile function during aging. Here we test the contribution of extracellular Ca2+ to contractile function of skeletal muscle during aging. First, we demonstrate graded coupling between SR Ca2+ release channel-mediated Ca2+ release and activation of SOCE. Inhibition of SOCE produced significant reduction of contractile force in young skeletal muscle, particularly at high frequency stimulation, and such effects were completely absent in aged skeletal muscle. Our data indicate that SOCE contributes to the normal physiological contractile response of young healthy skeletal muscle and that defective extracellular Ca2+ entry through SOCE contributes to the reduced contractile force characteristic of aged skeletal muscle.
publisher	Impact Journals LLC
publishDate	2011
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164370/
_version_	1611473240423661568

Store-Operated Ca2+ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle

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