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Regulation of store-operated Ca~(2+) entry by CD38 in human airway smooth muscle

机译：CD38对人气道平滑肌中钙操纵的Ca〜（2+）进入的调节

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First published January 4, 2008; doi: 10.1152/ajplung.00394.2007.-The ectoenzyme CD38 catalyzes synthesis and degradation of cyclic ADP ribose in airway smooth muscle (ASM). The proinflammatory cytokine TNFa, which enhances agonist-induced intracellular Ca~(2+) ([Ca~(2+)]i responses, has been previously shown to increases CD38 expression. In the present study, we tested the hypothesis that the effects of TNFa on CD38 expression vs. changes in [Ca~(2+)]i regulation in ASM cells are linked. Using isolated human ASM cells, CD38 expression was either increased (transfection) or knocked down [small interfering RNA (siRNA)], and [Ca~(2+)]i responses to sarcoplasmic reticulum depletion [i.e., store-operated Ca~(2+) entry (SOCE)] were evaluated in the presence vs. absence of TNFa. Results confirmed that TNFa significantly increased CD38 expression and ADP-ribosyl cyclase activity, an effect inhibited by CD38 siRNA, but unaltered by CD38 overexpres-sion. CD38 suppression blunted, whereas overexpression enhanced, ACh-induced [Ca~(2+)]i responses. TNFa-induced enhancement of [Ca~(2+)]i response to agonist was blunted by CD38 suppression, but enhanced by CD38 overexpression. Finally, TNFa-induced increase in SOCE was blunted by CD38 siRNA and potentiated by CD38 overexpression. Overall, these results indicate a critical role for CD38 in TNFa-induced enhancement of [Ca~(2+)]i in human ASM cells, and potentially to TNFa augmentation of airway responsiveness.
机译：首次发布时间：2008年1月4日; doi：10.1152 / ajplung.00394.2007.-外部酶CD38催化气道平滑肌（ASM）中环状ADP核糖的合成和降解。促炎细胞因子TNFa可增强激动剂诱导的细胞内Ca〜（2+）（[Ca〜（2 +）] i反应，先前已显示可增加CD38的表达。在本研究中，我们检验了这种效应的假设TNFa对CD38表达的影响与ASM细胞中[Ca〜（2 +）] i调节的变化之间的联系。使用分离的人ASM细胞，CD38表达要么增加（转染）要么被敲除[小干扰RNA（siRNA）] ，和[Ca〜（2 +）] i对肌浆网耗竭的反应[即，存储操作的Ca〜（2+）进入（SOCE）]在存在或不存在TNFa的情况下进行了评估，结果证实TNFa显着增加CD38的表达和ADP-核糖基环化酶活性受CD38 siRNA抑制，但不受CD38过表达影响; CD38抑制减弱，而过表达增强，ACh诱导的[Ca〜（2 +）] i反应; TNFa诱导的增强。 CD38抑制钝化[Ca〜（2 +）] i对激动剂的反应，但通过CD38过表达增强ession。最后，TNFα诱导的SOCE升高被CD38 siRNA抑制，并被CD38过表达增强。总体而言，这些结果表明，CD38在人ASM细胞中TNFa诱导的[Ca〜（2 +）] i增强中起关键作用，并可能对TNFa增强气道反应性起重要作用。

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