Journal
NATURE CELL BIOLOGY
Volume 7, Issue 5, Pages 525-530Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb1254
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Funding
- NCI NIH HHS [R01-CA95739] Funding Source: Medline
- NHLBI NIH HHS [R01-HL69000] Funding Source: Medline
- NIA NIH HHS [R01-AG15556] Funding Source: Medline
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Most excitable cells maintain tight control of intracellular Ca2+ through coordinated interaction between plasma membrane and endoplasmic or sarcoplasmic reticulum. Quiescent sarcoplasmic reticulum Ca2+ release machinery is essential for the survival and normal function of skeletal muscle(1-3). Here we show that subtle membrane deformations induce Ca2+ sparks in intact mammalian skeletal muscle. Spontaneous Ca2+ sparks can be reversibly induced by osmotic shock, and participate in a normal physiological response to exercise. In dystrophic muscle with fragile membrane integrity, stress-induced Ca2+ sparks are essentially irreversible. Moreover, moderate exercise in mdx muscle alters the Ca2+ spark response. Thus, membrane-deformation- induced Ca2+ sparks have an important role in physiological and pathophysiological regulation of Ca2+ signalling, and uncontrolled Ca2+ spark activity in connection with chronic activation of store-operated Ca2+ entry may function as a dystrophic signal in mammalian skeletal muscle.
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