Store‐operated calcium entry is required for sustained contraction and Ca2+ oscillations of airway smooth muscle

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp7419-list-0001">Airway hyper‐responsiveness in asthma is driven by excessive contraction of airway smooth muscle cells (ASMCs).Agonist‐induced Ca²⁺ oscillations underlie this contraction of ASMCs and the magnitude of this contraction is proportional to the Ca²⁺ oscillation frequency.Sustained contraction and Ca²⁺ oscillations require an influx of extracellular Ca²⁺, although the mechanisms and pathways mediating this Ca²⁺ influx during agonist‐induced ASMC contraction are not well defined.By inhibiting store‐operated calcium entry (SOCE) or voltage‐gated Ca²⁺ channels (VGCCs), we show that SOCE, rather than Ca²⁺ influx via VGCCs, provides the major Ca²⁺ entry pathway into ASMCs to sustain ASMCs contraction and Ca²⁺ oscillations.SOCE may therefore serve as a potential target for new bronchodilators to reduce airway hyper‐responsiveness in asthma.