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Am J Physiol Lung Cell Mol Physiol (January 4, 2008). doi:10.1152/ajplung.00394.2007
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Submitted on September 21, 2007
Accepted on December 28, 2007

REGULATION OF STORE-OPERATED Ca2+ ENTRY BY CD38 IN HUMAN AIRWAY SMOOTH MUSCLE

Gary C. Sieck1*, Thomas A. White1, Michael A Thompson2, Christina M Pabelick3, Mark E. Wylam4, and Y. S. Prakash3

1 Department of Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota, United States
2 Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota, United States
3 Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota, United States; Department of Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota, United States
4 Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, Minnesota, United States; Department of Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota, United States

* To whom correspondence should be addressed. E-mail: sieck.gary{at}mayo.edu.

The ectoenzyme CD38 catalyzes synthesis and degradation of cyclic-ADP-ribose (cADPR) in airway smooth muscle (ASM). The pro-inflammatory cytokine TNF-alpha (TNF{alpha}), which enhances agonist-induced intracellular Ca2+ ([Ca2+]i) responses, has been previously shown to increases CD38 expression. In the present study, we tested the hypothesis that the effects of TNF{alpha} on CD38 expression vs. changes in [Ca2+]i regulation in ASM cells are linked. Using isolated human ASM cells, CD38 expression was either increased (transfection) or knocked down (small interference RNA; siRNA), and [Ca2+]i responses to sarcoplasmic reticulum (SR) depletion (i.e. store-operated Ca2+ entry; SOCE) were evaluated in the presence vs. absence of TNF{alpha}. Results confirmed that TNF{alpha} significantly increased CD38 expression and ADP-ribosyl cyclase activity, an effect inhibited by CD38 siRNA, but unaltered by CD38 overexpression. CD38 suppression blunted, while overexpression enhanced, ACh-induced [Ca2+]i responses. TNF{alpha}-induced enhancement of [Ca2+]i response to agonist was blunted by CD38 suppression, but enhanced by CD38 overexpression. Finally, TNF{alpha}-induced increase in SOCE was blunted by CD38 siRNA, and potentiated by CD38 overexpression. Overall, these results indicate a critical role for CD38 in TNF{alpha} induced enhancement of [Ca2+]i in human ASM cells, and potentially to TNF{alpha} augmentation of airway responsiveness.




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