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Fluorescence-based Measurement of Store-operated Calcium Entry in Live Cells: from Cultured Cancer Cell to Skeletal Muscle Fiber
Published on: February 13, 2012
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Calcium entry units (CEUs): perspectives in skeletal muscle function and disease
Feliciano Protasi1,2, Laura Pietrangelo3,4, Simona Boncompagni3,5
1CAST, Center for Advanced Studies and Technology, University G. d'Annunzio of Chieti-Pescara, 66100, Chieti, Italy. feliciano.protasi@unich.it.
Journal of Muscle Research and Cell Motility
|August 20, 2020
Summary
Exercise promotes new Ca2+ Entry Units (CEUs) in skeletal muscle, enhancing fatigue resistance. These dynamic junctions, formed by STIM1 and ORAI1, improve calcium recovery and muscle function during activity.
Area of Science:
- Cellular Biology
- Muscle Physiology
- Calcium Signaling
Background:
- Store-operated Ca2+ entry (SOCE) is a vital cellular mechanism for calcium recovery, crucial in skeletal muscle for limiting fatigue.
- SOCE involves STIM1 (SR Ca2+ sensor) and ORAI1 (plasma membrane Ca2+ channel) interaction, particularly in transverse tubules (TTs).
Purpose of the Study:
- To investigate the role of exercise in skeletal muscle SOCE and identify novel structures involved in this process.
- To understand the formation and function of exercise-induced Ca2+ Entry Units (CEUs) and their impact on muscle fatigue.
Main Methods:
- Microscopy and molecular biology techniques to identify and characterize novel cellular junctions in skeletal muscle.
- Functional assays to assess Ca2+ entry and muscle fatigue resistance in response to exercise.
Main Results:
- Exercise induces the assembly of new intracellular junctions, termed Ca2+ Entry Units (CEUs), containing colocalized STIM1 and ORAI1.
- The presence of CEUs enhances Ca2+ entry via ORAI1, leading to improved fatigue resistance during repetitive muscle stimulation.
- CEUs are dynamic structures that assemble during activity and disassemble during recovery, involving SR plasticity and TT remodeling.
Conclusions:
- Exercise actively promotes the formation of CEUs, a novel organelle enhancing SOCE and muscle fatigue resistance.
- Dysfunctional SOCE or mutations in STIM1, ORAI1, or calsequestrin may contribute to tubular aggregate myopathy (TAM) and the formation of tubular aggregates (TAs).
- Further research is needed to elucidate the precise molecular triggers for CEU formation and the link between SOCE dysfunction and TA development in aging and disease.
Keywords:
Sarcoplasmic reticulum (SR)Store-operated Ca2+ entry (SOCE)Transverse tubules (TT)Tubular aggregate myopathy (TAM)More Related Videos
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