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1 Departments of Anesthesiology and Internal Medicine, Signal Transduction Laboratory, Rochester, MN, USA
2 Department of Physiology, Mayo Clinic and Foundation, Rochester, MN, USA
3 Trudeau Institute, Saranac Lake, NY, USA
* To whom correspondence should be addressed. E-mail: Chini.eduardo{at}mayo.edu.
Oxytocin-induced Ca2+ transients play an important role in myometrial contractions. Here using a knockout
model we found that the enzyme CD38, responsible for the synthesis of the second messenger cADPR (cyclic-
ADP-ribose), plays an important role on the oxytocin-induced Ca2+ transients and contraction. We also observed
that CD38 is necessary for tumor necrosis factor (TNF-
) increased agonist stimulated Ca2+ transients in human
myometrial cells. We provide experimental evidences that the TNF- effect is mediated by increased
expression of the enzyme CD38. First we observed that TNF- increased oxytocin induced Ca2+ transients and
CD38 expression in human myometrial cells. Furthermore, using siRNA (small interference RNA) technology
we observed that TNF- stimulation of agonist-induced Ca2+ transients was abolished by blocking the
expression of CD38. In control experiments we observed that activation of the component of the TNF-
signaling pathway NF
B was not affected by the treatments. Finally, we observed that the effects of TNF-
upon CD38 cyclase and oxytocin-induced Ca2+ transients are abolished by progesterone. In conclusion, we
provide the first experimental evidences that CD38 is important for myometrial Ca2+ transients and contraction.
Furthermore, CD38 is necessary for the TNF- mediated augmentation of agonist-induced Ca2+ transients in
myometrial cells. We propose that the balance between cytokines and placental steroids regulate the expression
of CD38 in vivo, and cell responsiveness to oxytocin.
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