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Updated: Jul 5, 2026
14:18
Fluorescence-based Measurement of Store-operated Calcium Entry in Live Cells: from Cultured Cancer Cell to Skeletal Muscle Fiber
Published on: February 13, 2012
Compromised store-operated Ca2+ entry in aged skeletal muscle
Xiaoli Zhao1, Noah Weisleder, Angela Thornton
1Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.
Aging Cell
|May 29, 2008
Summary
Aging impairs skeletal muscle function by reducing store-operated calcium entry (SOCE). This calcium regulation issue, linked to decreased mitsugumin-29, contributes to muscle weakness in older mice.
Area of Science:
- Muscle physiology
- Cellular biology
- Aging research
Background:
- Aging skeletal muscle exhibits weakness not fully explained by contractile machinery changes.
- Extracellular calcium (Ca2+) entry is altered in aged nonexcitable and excitable cells.
Purpose of the Study:
- To investigate the functional status of store-operated calcium entry (SOCE) in aged mouse skeletal muscle.
- To determine if reduced SOCE contributes to age-related muscle weakness.
Main Methods:
- Utilized Mn2+ quenching of Fura-2 fluorescence in aged (26-27 months) and young (2-5 months) mouse skeletal muscle fibers.
- Employed confocal-microscopic imaging to analyze Ca2+ movement within transverse tubules.
- Assessed expression levels of STIM1 and Orai mRNA, and mitsugumin-29 in aged and young muscle fibers.
Main Results:
- SOCE was found to be severely compromised in skeletal muscle fibers from aged mice compared to young mice.
- Reduced SOCE in aged muscle was not attributed to altered STIM1 expression or Orai mRNA levels.
- The reduction in SOCE was replicated in young mice lacking mitsugumin-29, a protein downregulated in aged muscle.
Conclusions:
- Decreased mitsugumin-29 expression in aged skeletal muscle is associated with reduced SOCE.
- Compromised SOCE and diminished mitsugumin-29 may contribute to impaired intracellular calcium homeostasis in aging muscle.
- These findings offer insights into the molecular mechanisms underlying age-related muscle weakness.
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