Impaired Ca2+ Store Functions in Skeletal and Cardiac Muscle Cells from Sarcalumenin-deficient Mice

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,...

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Published in:The Journal of biological chemistry 2005-02, Vol.280 (5), p.3500-3506
Main 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
Format: Article
Language:English
Subjects:
Animals
Calcium - metabolism
Heart - physiopathology
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Microscopy, Electron
Muscle Contraction
Muscle Fibers, Skeletal - metabolism
Muscle Fibers, Skeletal - pathology
Muscle Fibers, Skeletal - ultrastructure
Muscle, Skeletal - pathology
Muscle, Skeletal - physiopathology
Myocardial Contraction
Myocardium - metabolism
Myocardium - pathology
Myocytes, Cardiac - metabolism
Myocytes, Cardiac - pathology
Myocytes, Cardiac - ultrastructure
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Summary: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.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.M406618200