TY - JOUR
T1 - Impaired Ca2+ store functions in skeletal and cardiac muscle cells from sarcalumenin-deficient mice
AU - Yoshida, Morikatsu
AU - Minamisawa, Susumu
AU - Shimura, Miei
AU - Komazaki, Shinji
AU - Kume, Hideaki
AU - Zhang, Miao
AU - Matsumura, Kiyoyuki
AU - Nishi, Miyuki
AU - Saito, Minori
AU - Saeki, Yasutake
AU - Ishikawa, Yoshihiro
AU - Yanagisawa, Teruyuki
AU - Takeshima, Hiroshi
PY - 2005/2/4
Y1 - 2005/2/4
N2 - 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 Minen 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 electrocardiograpliy, 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.
AB - 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 Minen 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 electrocardiograpliy, 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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U2 - 10.1074/jbc.M406618200
DO - 10.1074/jbc.M406618200
M3 - Article
C2 - 15569689
AN - SCOPUS:13544266175
VL - 280
SP - 3500
EP - 3506
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
SN - 0021-9258
IS - 5
ER -