Impaired Ca2+ store functions in skeletal and cardiac muscle cells from sarcalumenin-deficient mice

Morikatsu Yoshida, Susumu Minamisawa, Miei Shimura, Shinji Komazaki, Hideaki Kume, Miao Zhang, Kiyoyuki Matsumura, Miyuki Nishi, Minori Saito, Yasutake Saeki, Yoshihiro Ishikawa, Teruyuki Yanagisawa, Hiroshi Takeshima

Research output: Contribution to journalArticlepeer-review

55 Citations (Scopus)

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 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.

Original languageEnglish
Pages (from-to)3500-3506
Number of pages7
JournalJournal of Biological Chemistry
Volume280
Issue number5
DOIs
Publication statusPublished - 2005 Feb 4

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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