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Calsequestrin Accumulation in Rough Endoplasmic Reticulum Promotes Perinuclear Ca2+ Release
Journal article   Open access   Peer reviewed

Calsequestrin Accumulation in Rough Endoplasmic Reticulum Promotes Perinuclear Ca2+ Release

Ang Guo, Steven E. Cala and Long-Sheng Song
The Journal of biological chemistry, Vol.287(20), pp.16670-16680
05/11/2012
DOI: 10.1074/jbc.M112.340927
PMCID: PMC3351355
PMID: 22457350
url
https://doi.org/10.1074/jbc.M112.340927View
Published (Version of record) Open Access

Abstract

Molecular mechanisms underlying Ca2+ regulation by perinuclear endoplasmic/sarcoplasmic reticulum (ER/SR) cisternae in cardiomyocytes remain obscure. To investigate the mechanisms of changes in cardiac calsequestrin ( CSQ2) trafficking on perinuclear Ca2+ signaling, we manipulated the subcellular distribution of CSQ2 by overexpression of CSQ2-DsRed, which specifically accumulates in the perinuclear rough ER. Adult ventricular myocytes were infected with adenoviruses expressing CSQ2-DsRed, CSQ2-WT, or empty vector. We found that perinuclear enriched CSQ2-DsRed, but not normally distributed CSQ2-WT, enhanced nuclear Ca2+ transients more potently than cytosolic Ca2+ transients. Overexpression of CSQ2-DsRed produced more actively propagating Ca2+ waves from perinuclear regions than did CSQ2-WT. Activities of the SR/ER Ca2+-ATPase and ryanodine receptor type 2, but not inositol 1,4,5-trisphosphate receptor type 2, were required for the generation of these perinuclear initiated Ca2+ waves. In addition, CSQ2-DsRed was more potent than CSQ2-WT in inducing cellular hypertrophy in cultured neonatal cardiomyocytes. Our data demonstrate for the first time that CSQ2 retention in the rough ER/perinuclear region promotes perinuclear Ca2+ signaling and predisposes to ryanodine receptor type 2-mediated Ca2+ waves from CSQ2-enriched perinuclear compartments and myocyte hypotrophy. These findings provide new insights into the mechanism of CSQ2 in Ca2+ homeostasis, suggesting that rough ER-localized Ca2+ stores can operate independently in raising levels of cytosolic/nucleoplasmic Ca2+ as a source of Ca2+ for Ca2+-dependent signaling in health and disease.
Biochemistry & Molecular Biology Life Sciences & Biomedicine Science & Technology

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