Upregulation of store-operated Ca2+ entry in dystrophic mdx mouse muscle

Edwards, Joshua N., Friedrich, Oliver, Cully, Tanya R., von Wegner, Frederic, Murphy, Robyn M. and Launikonis, Bradley S. (2010) Upregulation of store-operated Ca2+ entry in dystrophic mdx mouse muscle. American Journal of Physiology: Cell Physiology, 299 1: C42-C50. doi:10.1152/ajpcell.00524.2009


Author Edwards, Joshua N.
Friedrich, Oliver
Cully, Tanya R.
von Wegner, Frederic
Murphy, Robyn M.
Launikonis, Bradley S.
Title Upregulation of store-operated Ca2+ entry in dystrophic mdx mouse muscle
Formatted title
Upregulation of store-operated Ca2+ entry in dystrophic mdx mouse muscle
Journal name American Journal of Physiology: Cell Physiology   Check publisher's open access policy
ISSN 0363-6143
1522-1563
Publication date 2010-07
Sub-type Article (original research)
DOI 10.1152/ajpcell.00524.2009
Volume 299
Issue 1
Start page C42
End page C50
Total pages 9
Place of publication Bethesda, MD, United States
Publisher American Physiology Society
Collection year 2011
Language eng
Formatted abstract
Store-operated Ca2+ entry (SOCE) is an important mechanism in virtually all cells. In adult skeletal muscle, this mechanism is highly specialized for the rapid delivery of Ca2+ from the transverse tubule into the junctional cleft during periods of depleting Ca2+ release. In dystrophic muscle fibers, SOCE may be a source of Ca2+ overload, leading to cell necrosis. However, this possibility is yet to be examined in an adult fiber during Ca2+ release. To examine this, Ca2+ in the tubular system and cytoplasm were simultaneously imaged during direct release of Ca2+ from sarcoplasmic reticulum (SR) in skeletal muscle fibers from healthy (wild-type, WT) and dystrophic mdx mouse. The mdx fibers were found to have normal activation and deactivation properties of SOCE. However, a depression of the cytoplasmic Ca2+ transient in mdx compared with WT fibers was observed, as was a shift in the SOCE activation and deactivation thresholds to higher SR Ca2+ concentrations ([Ca2+]SR). The shift in SOCE activation and deactivation thresholds was accompanied by an approximately three-fold increase in STIM1 and Orai1 proteins in dystrophic muscle. While the mdx fibers can introduce more Ca2+ into the fiber for an equivalent depletion of [Ca2+]SR via SOCE, it remains unclear whether this is deleterious.
Copyright © 2010 the American Physiological Society.
Keyword Skeletal muscle
Sarcoplasmic reticulum
Muscular dystrophy
STIM1
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2011 Collection
School of Biomedical Sciences Publications
 
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Created: Sun, 04 Jul 2010, 00:07:35 EST