Modulation of calcium signaling by interleukin-13 in human airway smooth muscle - Role of CD38/cyclic adenosine diphosphate ribose pathway

被引:113
作者
Deshpande, DA
Dogan, S
Walseth, TF
Miller, SM
Amrani, Y
Panettieri, RA
Kannan, MS
机构
[1] Univ Minnesota, Coll Vet Med, Dept Vet Pathobiol, St Paul, MN 55108 USA
[2] Univ Minnesota, Dept Pharmacol, St Paul, MN 55108 USA
[3] Mayo Clin, Dept Physiol, Rochester, MN USA
[4] Univ Penn, Sch Med, Dept Med, Philadelphia, PA 19104 USA
关键词
D O I
10.1165/rcmb.2003-0313OC
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
CD38/cyclic adenosine diphosphate ribose (cADPR) signaling plays an important role in the regulation of intracellular calcium responses to agonists in a variety of cells, including airway smooth muscle (ASM) cells. The present study was aimed at determining the effect of interleukin (IL)-13, a cytokine implicated in the pathogenesis of asthma, on CD38/cADPR signaling and to ascertain the contribution of CD38/cADPR signaling to IL-13-induced airway hyperresponsiveness. Human ASM cells maintained in culture were exposed to 50 ng/ml IL-13 for 22 h and levels of CD38 expression and intracellular calcium responses to agonists were measured. Treatment of human ASM cells with IL-13 resulted in increased CD38 expression as determined by real-time polymerase chain reaction, Western blot analysis, and indirect immunofluorescence. Increased CD38 expression was reflected as increased ADP-ribosyl cyclase activity in the ASM cell membranes. The net intracellular calcium responses to bradykinin, thrombin, and histamine were significantly (P less than or equal to 0.05) higher in cells treated with IL-13 compared with controls. Furthermore, 8-bromo-cADPR, a cADPR antagonist, attenuated IL-13-induced augmented intracellular calcium responses to agonists in human ASM cells. These findings indicate that the CD38/cADPRdependent pathway has a major role in IL-13-induced modulation of calcium signaling in human ASM.
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页码:36 / 42
页数:7
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