| First Author | Edwards JN | Year | 2010 |
| Journal | Am J Physiol Cell Physiol | Volume | 299 |
| Issue | 1 | Pages | C42-50 |
| PubMed ID | 20427714 | Mgi Jnum | J:162510 |
| Mgi Id | MGI:4819073 | Doi | 10.1152/ajpcell.00524.2009 |
| Citation | Edwards JN, et al. (2010) Upregulation of store-operated Ca2+ entry in dystrophic mdx mouse muscle. Am J Physiol Cell Physiol 299(1):C42-50 |
| abstractText | 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. |
