NDLI: Role of TRPC1 channel in skeletal muscle function

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zanou, Nadège Shapovalov, Georges Louis, Magali Tajeddine, Nicolas Gallo, Chiara Van Schoor, Monique Anguish, Isabelle Cao, My Linh Schakman, Olivier Dietrich, Alexander Lebacq, Jean Ruegg, Urs Roulet, Emmanuelle Birnbaumer, Lutz Gailly, Philippe
Description	Country affiliation: Belgium Author Affiliation: Zanou N ( Laboratory of Cell Physiology, Inst. of Neuroscience, Université Catholique de Louvain, 55/40 av. Hippocrate, 1200 Brussels, Belgium. philippe.gailly@uclouvain.be)
Abstract	Skeletal muscle contraction is reputed not to depend on extracellular Ca2+. Indeed, stricto sensu, excitation-contraction coupling does not necessitate entry of Ca2+. However, we previously observed that, during sustained activity (repeated contractions), entry of Ca2+ is needed to maintain force production. In the present study, we evaluated the possible involvement of the canonical transient receptor potential (TRPC)1 ion channel in this entry of Ca2+ and investigated its possible role in muscle function. Patch-clamp experiments reveal the presence of a small-conductance channel (13 pS) that is completely lost in adult fibers from TRPC1(-/-) mice. The influx of Ca2+ through TRPC1 channels represents a minor part of the entry of Ca(2+) into muscle fibers at rest, and the activity of the channel is not store dependent. The lack of TRPC1 does not affect intracellular Ca2+ concentration ([Ca2+](i)) transients reached during a single isometric contraction. However, the involvement of TRPC1-related Ca2+ entry is clearly emphasized in muscle fatigue. Indeed, muscles from TRPC1(-/-) mice stimulated repeatedly progressively display lower [Ca2+](i) transients than those observed in TRPC1(+/+) fibers, and they also present an accentuated progressive loss of force. Interestingly, muscles from TRPC1(-/-) mice display a smaller fiber cross-sectional area, generate less force per cross-sectional area, and contain less myofibrillar proteins than their controls. They do not present other signs of myopathy. In agreement with in vitro experiments, TRPC1(-/-) mice present an important decrease of endurance of physical activity. We conclude that TRPC1 ion channels modulate the entry of Ca(2+) during repeated contractions and help muscles to maintain their force during sustained repeated contractions.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
DOI	10.1152/ajpcell.00241.2009
Journal	American Journal of Physiology - Cell Physiology
Issue Number	1
Volume Number	298
Language	English
Publisher	American Physiological Society
Publisher Date	2010-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Muscle, Skeletal Physiology Trpc Cation Channels Animals Calcium Metabolism Cyclophilins Genetics Dna Primers Gene Amplification Heterozygote Isometric Contraction Mice Mice, Knockout Muscle Contraction Muscle Fatigue Muscle Fibers, Skeletal Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Deficiency Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
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