Impaired Ca2+ store functions in skeletal and cardiac muscle cells from sarcalumenin-deficient mice |
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Authors: | Yoshida Morikatsu Minamisawa Susumu Shimura Miei Komazaki Shinji Kume Hideaki Zhang Miao Matsumura Kiyoyuki Nishi Miyuki Saito Minori Saeki Yasutake Ishikawa Yoshihiro Yanagisawa Teruyuki Takeshima Hiroshi |
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Affiliation: | Medical Chemistry and Molecular Pharmacology, Tohoku University Graduate School of Medicine, Sendai, Miyagi 980-8575, Japan. |
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Abstract: | Sarcalumenin (SAR), specifically expressed in striated muscle cells, is a Ca2+-binding protein localized in the sarcoplasmic reticulum (SR) of the intracellular Ca2+ store. By generating SAR-deficient mice, we herein examined its physiological role. The mutant mice were apparently normal in growth, health, and reproduction, indicating that SAR is not essential for fundamental muscle functions. SAR-deficient skeletal muscle carrying irregular SR ultrastructures retained normal force generation but showed slow relaxation phases after contractions. A weakened Ca2+ uptake activity was detected in the SR prepared from mutant muscle, indicating that SAR contributes to Ca2+ buffering in the SR lumen and also to the maintenance of Ca2+ pump proteins. Cardiac myocytes from SAR-deficient mice showed slow contraction and relaxation accompanied by impaired Ca2+ transients, and the mutant mice exhibited a number of impairments in cardiac performance as determined in electrocardiography, ventricular catheterization, and echocardiography. The results obtained demonstrate that SAR plays important roles in improving the Ca2+ handling functions of the SR in striated muscle. |
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