Ryanodine receptor activity and store-operated Ca 2+ entry: Critical regulators of Ca 2+ content and function in skeletal muscle.

Autor: Pearce L; School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, Australia., Meizoso-Huesca A; School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, Australia., Seng C; School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, Australia., Lamboley CR; School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, Australia., Singh DP; School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, Australia., Launikonis BS; School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, Australia.
Jazyk: angličtina
Zdroj: The Journal of physiology [J Physiol] 2023 Oct; Vol. 601 (19), pp. 4183-4202. Date of Electronic Publication: 2022 Mar 16.
DOI: 10.1113/JP279512
Abstrakt: Store-operated Ca 2+ entry (SOCE) is critical to cell function. In skeletal muscle, SOCE has evolved alongside excitation-contraction coupling (EC coupling); as a result, it displays unique properties compared to SOCE in other cells. The plasma membrane of skeletal muscle is mostly internalized as the tubular system, with the tubules meeting the sarcoplasmic reticulum (SR) terminal cisternae, forming junctions where the proteins that regulate EC coupling and SOCE are positioned. In this review, we describe the properties and roles of SOCE based on direct measurements of Ca 2+ influx during SR Ca 2+ release and leak. SOCE is activated immediately and locally as the [Ca 2+ ] of the junctional SR terminal cisternae ([Ca 2+ ] jSR ) depletes. [Ca 2+ ] jSR changes rapidly and steeply with increasing activity of the SR ryanodine receptor isoform 1 (RyR1). The high fidelity of [Ca 2+ ] jSR with RyR1 activity probably depends on the SR Ca 2+ -buffer calsequestrin that is located immediately behind RyR1 inside the SR. This arrangement provides in-phase activation and deactivation of SOCE with a large dynamic range, allowing precise grading of SOCE flux. The in-phase activation of SOCE as the SR partially depletes traps Ca 2+ in the cytoplasm, preventing net Ca 2+ loss. Mild presentation of RyR1 leak can occur under physiological conditions, providing fibre Ca 2+ redistribution without changing fibre Ca 2+ content. This condition preserves normal contractile function at the same time as increasing basal metabolic rate. However, higher RyR1 leak drives excess cytoplasmic and mitochondrial Ca 2+ load, setting a deleterious intracellular environment that compromises the function of the skeletal muscle.
(© 2022 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)
Databáze: MEDLINE
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