Transcriptional regulation of CD38 expression by tumor necrosis factor‐α in human airway smooth muscle cells: role of NF‐κB and sensitivity to glucocorticoids

Kang, Bitna; Tirumurugaan, K.G.; Deshpande, Deepak A.; Amrani, Yassine; Panettieri, Reynold A.; Walseth, Timothy F.; Karman, Mathur S.

doi:10.1096/fj.05-4585fje

Cited by 61 publications

(71 citation statements)

References 49 publications

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“…Previous studies from our laboratory and from others using human ASM cells have implicated the CD38/cADPR signaling in [Ca 2ϩ ] i hyperresponsiveness to contractile agonists with possible relevance to inflammatory airway diseases (7,18,19,37). For example, increases in CD38 expression and activity are observed in human ASM cells exposed to IL-1␤, IFN-␥, TNF-␣, and IL-13.…”

mentioning

confidence: 84%

CD38-deficient mice have reduced airway hyperresponsiveness following IL-13 challenge

Guedes¹,

Paulin²,

Rivero-Nava³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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-The transmembrane glycoprotein CD38 in airway smooth muscle is the source of cyclic-ADP ribose, an intracellular calcium-releasing molecule, and is subject to regulatory effects of cytokines such as interleukin (IL)-13, a cytokine implicated in asthma. We investigated the role of CD38 in airway hyperresponsiveness using a mouse model of IL-13-induced airway disease. Wild-type (WT) and CD38-deficient (CD38KO) mice were intranasally challenged with 5 g of IL-13 three times on alternate days under isoflurane anesthesia. Lung resistance (RL) in response to inhaled methacholine was measured 24 h after the last challenge in pentobarbital-anesthetized, tracheostomized, and mechanically ventilated mice. Bronchoalveolar cytokines, bronchoalveolar and parenchymal inflammation, and smooth muscle contractility and relaxation using tracheal segments were also evaluated. Changes in methacholine-induced R L were significantly greater in the WT than in the CD38KO mice following intranasal IL-13 challenges. Airway reactivity after IL-13 exposure, as measured by the slope of the methacholine dose-response curve, was significantly higher in the WT than in the CD38KO mice. The rate of isometric force generation in tracheal segments (e.g., smooth muscle reactivity) was greater in the WT than in the CD38KO mice following incubation with IL-13. IL-13 treatment reduced isoproterenol-induced relaxations to similar magnitudes in tracheal segments obtained from WT and CD38KO mice. Both WT and CD38KO mice developed significant bronchoalveolar and parenchymal inflammation after IL-13 challenges compared with naïve controls. The results indicate that CD38 contributes to airway hyperresponsiveness in lungs exposed to IL-13 at least partly by increasing airway smooth muscle reactivity to contractile agonists. interleukin-13; inflammation; asthma; eosinophil; airway smooth muscle CD38 IS A MULTIFUNCTIONAL ECTOENZYME that catalyzes the conversion of ␤-nicotinamide adenine dinucleotide to cyclic ADP-ribose (cADPR) and ADP-ribose (16). Both CD38 and its product cADPR are present in airway smooth muscle (ASM) cells and other mammalian cell types (8,26,32,39). Together with inositol 1,4,5-trisphosphate, cADPR is an important mediator of intracellular calcium ([Ca 2ϩ ] i ) release in smooth muscle cells including that of the airways (7,20,31). The dynamics of [Ca 2ϩ ] i responses to stimuli are central in the regulation of ASM contraction, bronchomotor tone, and airway caliber (33). cADPR induces Ca 2ϩ release from the sarcoplasmic reticulum through activation of ryanodine receptor channels in ASM cells (31). The [Ca 2ϩ ] i responses of human ASM cells exposed to acetylcholine, thrombin, and bradykinin are reduced by the competitive cADPR antagonist 8-bromo-cADPR in a magnitude that correlates positively with the level of CD38 expression (6).CD38-deficient (CD38KO) mice have been used to elucidate the role of CD38 in the function of several organs. CD38-generated cADPR plays a critical role in Ca 2ϩ -induced insulin secretion (21), os...

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mentioning

confidence: 84%

CD38-deficient mice have reduced airway hyperresponsiveness following IL-13 challenge

Guedes¹,

Paulin²,

Rivero-Nava³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…However, they fall short of proving that IκBα induction plays no part in the antiinflammatory actions of GCs. IκBα expression is tissue-specifically regulated, and is enhanced by GCs in several primary or transformed cell types (Almon et al, 2005;Auphan et al, 1995;Kang et al, 2006;Kurata and Yamamoto, 1999;Kurokouchi et al, 2000;Quan et al, 2000;Ramdas and Harmon, 1998;Scheinman et al, 1995a;Shames et al, 1998;Stojadinovic et al, 2006;Thiele et al, 1999). In A c c e p t e d M a n u s c r i p t A Clark Anti-inflammatory functions of glucocorticoid-induced genes Page 17 of 53 some cases GC treatment inhibited IκBα degradation, nuclear translocation of p65 or formation of nuclear NFκB complexes (Eberhardt et al, 2002;Goppelt-Struebe et al, 2000;Kurata and Yamamoto, 1999;Kurokouchi et al, 2000;Ma et al, 2004;Mukaida et al, 1994;Vital et al, 2003).…”

Section: A Clarkmentioning

confidence: 99%

Anti-inflammatory functions of glucocorticoid-induced genes

Clark

2007

Molecular and Cellular Endocrinology

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“…Thus, these cytokines are finding increasing use as markers in the detection and prognostic assessment of cancer (21)(22)(23)(24)(25)(26)(27)(28)(29). Moreover, cytokines have been shown to enhance CD38 expression in different cell types (26).…”

Section: Cd38 Expression In Peripheric Mouse Lymphocytes In Culturementioning

confidence: 99%

CD38 expression as response of hematopoietic system to cancer

et al. 2011

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Abstract. Erythrocyte and lymphocyte NAD + glycohydrolase levels were previously found to be elevated in cancer patients. These results were confirmed in an animal model. The administration of live Ehrlich ascites tumor cells to BALB/c mice led to increases in erythrocyte and lymphocyte NAD + glycohydrolase, along with tumor development. Serum samples, ascites fluid from mice with developed tumors, serum samples from cancer patients and Ehrlich cell supernatants had a similar stimulatory effect when administered to mice or when incubated with peripheric lymphocytes in culture. These increases were accompanied by the appearance of an anti-CD38 reactive band of 45 kDa in SDS-PAGE/Western blot analyses of erythrocyte ghost and lymphocyte membrane proteins. The results, supported by flow cytometry data, support previous clinical findings that an enhancement in CD38 expression occurs in the hematopoietic system during proliferative processes. Moreover, they suggest that CD38 expression is triggered at least in part by a certain cytokine(s) secreted by cancer cells. Finally, the results emphasize the prospective use of CD38 expression as a marker of tumor development and progression.

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Transcriptional regulation of CD38 expression by tumor necrosis factor‐α in human airway smooth muscle cells: role of NF‐κB and sensitivity to glucocorticoids

Cited by 61 publications

References 49 publications

CD38-deficient mice have reduced airway hyperresponsiveness following IL-13 challenge

CD38-deficient mice have reduced airway hyperresponsiveness following IL-13 challenge

Anti-inflammatory functions of glucocorticoid-induced genes

CD38 expression as response of hematopoietic system to cancer

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