Evidence for an Intracellular ADP-ribosyl Cyclase/NAD+-glycohydrolase in Brain from CD38-deficient Mice

Ceni, Claire; Muller-Steffner, Hélène; Lund, Frances E.; Pochon, Nathalie; Schweitzer, Annie; Waard, Michel De; Schuber, Francis; Villaz, Michel; Moutin, Marie‐Jo

doi:10.1074/jbc.m301196200

Cited by 65 publications

(74 citation statements)

References 43 publications

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“…This seemingly contradictory result may be explained by the possibility that CD38-independent ADP-ribosyl cyclase can compensate the loss of CD38 to produce normal levels of cADPR, thereby contributing to the normal Ca 21 handling properties of these neurons. Along this line, it has been reported previously that an intracellular membrane-bound ADP-ribosyl cyclase/NAD 1 -glycohydrolase distinct from CD38 is expressed in mouse brain, and the novel enzyme is more active in the developing brain than in the adult tissue [27]. Thus, the search and identification of CD38-independent ADP-ribosyl cyclase must continue.…”

Section: Discussionmentioning

confidence: 93%

CD38 Is Required for Neural Differentiation of Mouse Embryonic Stem Cells by Modulating Reactive Oxygen Species

et al. 2015

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CD38 is a multifunctional membrane enzyme and the main mammalian ADP-ribosyl cyclase, which catalyzes the synthesis and hydrolysis of cADPR, a potent endogenous Ca 21 mobilizing messenger. Here, we explored the role of CD38 in the neural differentiation of mouse embryonic stem cells (ESCs). We found that the expression of CD38 was decreased during the differentiation of mouse ESCs initiated by adherent monoculture. Perturbing the CD38/cADPR signaling by either CD38 knockdown or treatment of cADPR antagonists inhibited the neural commitment of mouse ESCs, whereas overexpression of CD38 promoted it. Moreover, CD38 knockdown dampened reactive oxygen species (ROS) production during neural differentiation of ESCs by inhibiting NADPH oxidase activity, while CD38 overexpression enhanced it. Similarly, application of hydrogen peroxide mitigated the inhibitory effects of CD38 knockdown on neural differentiation of ESCs. Taken together, our data indicate that the CD38 signaling pathway is required for neural differentiation of mouse ESCs by modulating ROS production. STEM CELLS 2015; 33:2664-2673 SIGNIFICANCE STATEMENTThe in vitro generation of neural lineage cells from embryonic stem (ES) cells is a promising approach to produce cells suitable for neural tissue repair and cell-based replacement therapies of the nervous system. The functions regulated by the CD38 signaling are diverse. Here we found that the CD38 signaling pathway is required for neural differentiation of mouse ES cells by modulating ROS production. Our findings not only increase our understanding of ES cell differentiation and embryonic neural development, but also encourage the application of therapies based on ES cells in the treatment of neurological and psychiatric diseases.

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Section: Discussionmentioning

confidence: 93%

CD38 Is Required for Neural Differentiation of Mouse Embryonic Stem Cells by Modulating Reactive Oxygen Species

et al. 2015

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“…Investigators have reported ADP-ribosyl cyclase activity that is independent of CD38 (69). The non-CD38 ADP-ribosyl cyclase activity has been reported in brain homogenates obtained from CD38 knockout mice (69). However, CD38 is reported to be the only ADP-ribosyl cyclase present in the ASM (47).…”

Section: Adp-ribosyl Cyclase Cd38 and Cyclic Adp-ribose In Airway Smentioning

confidence: 99%

Calcium Signaling in Airway Smooth Muscle

Jude¹,

Wylam²,

Walseth³

et al. 2008

Proceedings of the American Thoracic Society

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Contractility of airway smooth muscle requires elevation of intracellular calcium concentration. Under resting conditions, airway smooth muscle cells maintain a relatively low intracellular calcium concentration, and activation of the surface receptors by contractile agonists results in an elevation of intracellular calcium, culminating in contraction of the cell. The pattern of elevation of intracellular calcium brought about by agonists is a dynamic process and involves the coordinated activities of ion channels located in the plasma membrane and the sarcoplasmic reticulum. Among the signaling molecules involved in this dynamic calcium regulation in airway smooth muscle cells are inositol 1,4,5-trisphosphate and cyclic ADPribose, which mobilize calcium from the sarcoplasmic reticulum by acting via the inositol 1,4,5-trisphosphate and ryanodine receptors, respectively. In addition, calcium influx from the extracellular space is critical for the repletion of the intracellular calcium stores during activation of the cells by agonists. Calcium influx can occur via voltage-and receptor-gated channels in the plasma membrane, as well as by influx that is triggered by depletion of the intracellular stores (i.e., store-operated calcium entry mechanism). Transient receptor potential proteins appear to mediate the calcium influx via receptor-and store-operated channels. Recent studies have shown that proinflammatory cytokines regulate the expression and activity of the pathways involved in intracellular calcium regulation, thereby contributing to airway smooth muscle cell hyperresponsiveness. In this review, we will discuss the specific roles of cyclic ADP-ribose/ryanodine receptor channels and transient receptor potential channels in the regulation of intracellular calcium in airway smooth muscle cells. DYNAMIC INTRACELLULAR CALCIUM REGULATION IN AIRWAY SMOOTH MUSCLE CELLSExposure of airway smooth muscle (ASM) cells to contractile agonists results in a biphasic elevation of intracellular calcium concentration ([Ca 21 ] i ) that is characterized by an initial rapid and transient rise in calcium, followed by a decline to a lower, sustained steady-state concentration above the basal level (1-3). This biphasic [Ca 21 ] i response results from calcium influx from the extracellular space and release of calcium from the intracellular stores (i.e., the sarcoplasmic reticulum [SR]). Earlier studies have attributed the initial rapid and transient phase of the [Ca 21 ] i response to release from the SR, while the sustained phase of the response was thought to be due to influx from the extracellular space (2-6). Recent investigations using the improved temporal and spatial resolution features of real-time confocal microscopy have shed light on the dynamics of the [Ca 21 ] i response in ASM cells. These studies have shown that the biphasic [Ca 21 ] i response of ASM cells elicited by contractile agonists in reality consists of propagating regenerative calcium oscillations that originate at a location within a cell and propagate...

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“…Mounting evidence has indicated that ADPR-cyclase(s) other than CD38 may exist in the kidney, brain, and the heart (40,45), including various cells (30,(45)(46)(47). The first clues to the existence of novel ADPR-cyclase(s) emerged from experiments of the comparison of tissue cADPR levels in CD38 wild type and knockout mice (40).…”

Section: Diabetic Nephropathy and The Renin-angiotensin-aldosterone Smentioning

confidence: 99%

Kidney ADP-Ribosyl Cyclase Inhibitors as a Therapeutic Tool for Diabetic Nephropathy

Kim¹

2012

Diabetic Nephropathy

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Evidence for an Intracellular ADP-ribosyl Cyclase/NAD+-glycohydrolase in Brain from CD38-deficient Mice

Cited by 65 publications

References 43 publications

CD38 Is Required for Neural Differentiation of Mouse Embryonic Stem Cells by Modulating Reactive Oxygen Species

CD38 Is Required for Neural Differentiation of Mouse Embryonic Stem Cells by Modulating Reactive Oxygen Species

Calcium Signaling in Airway Smooth Muscle

Kidney ADP-Ribosyl Cyclase Inhibitors as a Therapeutic Tool for Diabetic Nephropathy

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