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Am J Physiol Lung Cell Mol Physiol 286: L909-L917, 2004. First published November 14, 2003; doi:10.1152/ajplung.00317.2003
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EDITORIAL FOCUS

Store-operated Ca2+ entry in porcine airway smooth muscle

Binnaz Ay,1,2 Y. S. Prakash,1 Christina M. Pabelick,1 and Gary C. Sieck1,3

Departments of 1Anesthesiology and 3Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota 55905; and 2Department of Anesthesiology, Marmara University, 34660 Istanbul, Turkey

Submitted 11 September 2003 ; accepted in final form 10 November 2003

Ca2+ influx triggered by depletion of sarcoplasmic reticulum (SR) Ca2+ stores [mediated via store-operated Ca2+ channels (SOCC)] was characterized in enzymatically dissociated porcine airway smooth muscle (ASM) cells. When SR Ca2+ was depleted by either 5 µM cyclopiazonic acid or 5 mM caffeine in the absence of extracellular Ca2+, subsequent introduction of extracellular Ca2+ further elevated [Ca2+]i. SOCC was insensitive to 1 µM nifedipine- or KCl-induced changes in membrane potential. However, preexposure of cells to 100 nM–1 mM La3+ or Ni2+ inhibited SOCC. Exposure to ACh increased Ca2+ influx both in the presence and absence of a depleted SR. Inhibition of inositol 1,4,5-trisphosphate (IP)-induced SR Ca2+ release by 20 µM xestospongin D inhibited SOCC, whereas ACh-induced IP3 production by 5 µM U-73122 had no effect. Inhibition of Ca2+ release through ryanodine receptors (RyR) by 100 µM ryanodine also prevented Ca2+ influx via SOCC. Qualitatively similar characteristics of SOCC-mediated Ca2+ influx were observed with cyclopiazonic acid- vs. caffeine-induced SR Ca2+ depletion. These data demonstrate that a Ni2+/La3+-sensitive Ca2+ influx via SOCC in porcine ASM cells involves SR Ca2+ release through both IP3 and RyR channels. Additional regulation of Ca2+ influx by agonist may be related to a receptor-operated, noncapacitative mechanism.

sarcoplasmic reticulum; calcium release-activated calcium channel; inositol trisphosphate; ryanodine; acetylcholine


Address for reprint requests and other correspondence: Y. S. Prakash, 4-184 W Jos SMH, Mayo Clinic, Rochester, MN 55905 (E-mail: prakash.ys{at}mayo.edu).




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