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

Edwards JN, Friedrich O, Cully TR, von Wegner F, Murphy RM, Launikonis BS (2010)

Publication Language: English

Publication Status: Published

Publication Type: Journal article, Original article

Publication year: 2010

Journal

American journal of physiology. Cell physiology

Book Volume: 299

Pages Range: C42-50

Journal Issue: 1

URI: http://ajpcell.physiology.org/content/299/1/C42

DOI: 10.1152/ajpcell.00524.2009

Open Access Link: http://ajpcell.physiology.org/content/299/1/C42.full-text.pdf+html

Abstract

Store-operated Ca(2+) entry (SOCE) is an important mechanism in virtually all cells. In adult skeletal muscle, this mechanism is highly specialized for the rapid delivery of Ca(2+) from the transverse tubule into the junctional cleft during periods of depleting Ca(2+) release. In dystrophic muscle fibers, SOCE may be a source of Ca(2+) overload, leading to cell necrosis. However, this possibility is yet to be examined in an adult fiber during Ca(2+) release. To examine this, Ca(2+) in the tubular system and cytoplasm were simultaneously imaged during direct release of Ca(2+) 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 Ca(2+) transient in mdx compared with WT fibers was observed, as was a shift in the SOCE activation and deactivation thresholds to higher SR Ca(2+) concentrations ([Ca(2+)](SR)). The shift in SOCE activation and deactivation thresholds was accompanied by an approximately threefold increase in STIM1 and Orai1 proteins in dystrophic muscle. While the mdx fibers can introduce more Ca(2+) into the fiber for an equivalent depletion of [Ca(2+)](SR) via SOCE, it remains unclear whether this is deleterious.

Authors with CRIS profile

Oliver Friedrich Lehrstuhl für Medizinische Biotechnologie

Related research project(s)

Membrane Excitability and Cellular Calcium Regulation in the peripheral Nervous System under different (patho)-physiological Conditions and in Inflammatory Disease (ARC International Linkage Fellowship) April 1, 2008 - March 31, 2009

Involved external institutions

University of Queensland AU Australia (AU) La Trobe University AU Australia (AU) Goethe-Universität Frankfurt am Main DE Germany (DE)

How to cite

APA:

Edwards, J.N., Friedrich, O., Cully, T.R., von Wegner, F., Murphy, R.M., & Launikonis, B.S. (2010). Upregulation of store-operated Ca2+ entry in dystrophic mdx mouse muscle. American journal of physiology. Cell physiology, 299(1), C42-50. https://doi.org/10.1152/ajpcell.00524.2009

MLA:

Edwards, Joshua N., et al. "Upregulation of store-operated Ca2+ entry in dystrophic mdx mouse muscle." American journal of physiology. Cell physiology 299.1 (2010): C42-50.

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