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Papers In Press, published online ahead of print May 13, 2005
J. Biol. Chem, 10.1074/jbc.M502905200
Submitted on March 16, 2005
Revised on May 11, 2005
Accepted on May 13, 2005

Ryanodine receptors in muscarinic receptor-mediated Bronchoconstriction

Wanglei Du, Jonathan A. Stiber, Rosenberg B. Paul, Meissner Gerhard, and Jerry P. Eu

Department of Medicine, Duke University Medical Center, Durham, NC 27710

Corresponding Author: eu000001{at}duke.edu

Ryanodine receptors - intracellular calcium release channels essential for skeletal and cardiac muscle contraction - are also expressed in various types of smooth muscle cells. In particular, recent studies have suggested that in airway smooth muscle cells provoked by spasmogens, stored calcium release by the cardiac isoform of ryanodine receptor (RyR2) contributes to the calcium response that leads to airway constriction (bronchoconstriction). Here we report that mouse airway smooth muscle cells also express the skeletal muscle and brain isoforms of ryanodine receptors (RyR1 and RyR3, respectively). In these cells, RyR1 is localized to the periphery near the cell membrane whereas RyR3 is more centrally localized. Moreover, RyR1 and/or RyR3 in mouse airway smooth muscle also appear to mediate bronchoconstriction caused by the muscarinic receptor agonist carbachol. Inhibiting all ryanodine receptor isoforms with = 200 µM ryanodine attenuated the graded carbachol-induced contractile responses of mouse bronchial rings and calcium responses of airway smooth muscle cells throughout the range of carbachol used (50 nM to = 3 µM). In contrast, inhibiting only RyR1 and RyR3 with 25 µM dantrolene attenuated these responses caused by high (> 500 nM) but not by low concentrations of carbachol. These data suggest that, as the stimulation of muscarinic receptor in the airway smooth muscle increases, RyR1 and/or RyR3 also mediate the calcium response and thus bronchoconstriction. Our findings provide new insights into the complex calcium signaling in airway smooth muscle cells and suggest that ryanodine receptors are potential therapeutic targets in bronchospastic disorders such as asthma.


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