Metabolism and Actions of ADP-Riboses in Coronary Arterial Smooth Muscle

Li, Pinlan; Zou, Ai-Ping; Campbell, William B.

doi:10.1007/978-1-4419-8632-0_56

Cited by 23 publications

(20 citation statements)

References 8 publications

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“…In contrast, CADPR (10 M)-induced Ca 2ϩ release was shown to be resistant to heparin (10 g/ml), which is nevertheless able to fully inhibit the InsP 3 effect (Barone et al, 2002). It was observed in inside-out plasma membrane patches that cADPR (1-10 M) concentration-dependently reduces K Ca P o by up to 75% (Li et al, 1997).…”

Section: Pharmacological Modulation Of Smooth Muscle Srmentioning

confidence: 90%

Pharmacological Modulation of Sarcoplasmic Reticulum Function in Smooth Muscle

2004

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Section: Pharmacological Modulation Of Smooth Muscle Srmentioning

confidence: 90%

Pharmacological Modulation of Sarcoplasmic Reticulum Function in Smooth Muscle

2004

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“…The components of this pathway are present and functional in myometrial, vascular and airway smooth muscle cells (18)(19)(20)(21)(22)(23)(24). One important observation is the fact that the intracellular Ca 2+ transients induced by oxytocin are dependent on both the CD38/cADPR signaling pathway and extracellular Ca 2+ in human myometrial cells.…”

Section: Role Of Cadpr In Agonist-stimulated Ca 2+ Transientsmentioning

confidence: 99%

Modulation of store-operated Ca2+ entry by cyclic-ADP-ribose

Thompson

White

Chini

2006

Braz J Med Biol Res

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Store-operated Ca 2+ entry plays an important role in Ca 2+ homeostasis in cells but the mechanisms of control of these channels are not completely understood. We describe an investigation of the role of the CD38-cyclic-ADP-ribose (cADPR)-ryanodine-channel (RyR) signaling pathway in store-operated Ca 2+ entry in human smooth muscle. We observed that human myometrial cells have a functional storeoperated Ca 2+ entry mechanism. Furthermore, we observed the presence of transient receptor potential 1, 3, 4, 5, and 6 ion channels in human myometrial cells. Store-operated Ca 2+ transient was inhibited by at least 50-70% by several inhibitors of the RyR, including ryanodine (10 µM), dantrolene (10 µM), and ruthenium red (10 µM). Furthermore, the cell permeable inhibitor of the cADPR-system, 8-Br-cADPR (100 µM), is a potent inhibitor of the store-operated entry, decreasing the store operated entry by 80%. Pre-incubation of cells with 100 µM cADPR and the hydrolysis-resistant cADPR analog 3-deaza-cADPR (50 µM), but not with ADP-ribose (ADPR) leads to a 1.6-fold increase in the store-operated Ca 2+ transient. In addition, we observed that nicotinamide (1-10 mM), an inhibitor of cADPR synthesis, also leads to inhibition of the store-operated Ca 2+ transient by 50-80%. Finally, we observed that the transient receptor potential channels, RyR, and CD38 can be co-immunoprecipitated, indicating that they interact in vivo. Our observations clearly implicate the CD38-cADPR-ryanodine signaling pathway in the regulation of storeoperated Ca 2+ entry in human smooth muscle cells.

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“…Elevation of intracellular cADPR levels followed by Ca 2ϩ mobilizition and activation of Ca 2ϩ -dependent effects within cells has been found to be essential for versatile physiological processes, such as cell cycle regulation, cell proliferation, gene expression, egg fertilization, neurotransmitter release, muscle contraction, and nitric oxide signaling (10,29,55). Recent studies (17,35,36,52,55,57) in our laboratory and by others have reported that in vascular smooth muscle (VSM), cADPR production participates in its constrictor response to Ins(1,4,5)P 3 -independent agonists, such as acetylcholine, oxotremorine, 5-hydroxytryptamine, and endothelin, and these actions of cADPR are associated with activation of RyRs and consequent Ca 2ϩ mobilization. However, so far it remains unclear whether cADPR is involved in the regulation of endothelial function, in particular, in participating in endothelial NO-dependent vasodilator response.…”

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confidence: 99%

Cyclic ADP ribose-mediated Ca²⁺signaling in mediating endothelial nitric oxide production in bovine coronary arteries

Guo¹,

Teggatz²,

Zhang³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. Cyclic ADP ribosemediated Ca 2ϩ signaling in mediating endothelial nitric oxide production in bovine coronary arteries. Am J Physiol Heart Circ Physiol 290: H1172-H1181, 2006. First published October 21, 2005 doi:10.1152/ajpheart.00441.2005.-The present study tested the hypothesis that cyclic ADP ribose (cADPR) serves as a novel second messenger to mediate intracellular Ca 2ϩ mobilization in coronary arterial endothelial cells (CAECs) and thereby contributes to endothelium-dependent vasodilation. In isolated and perfused small bovine coronary arteries, bradykinin (BK)-induced concentrationdependent vasodilation was significantly attenuated by 8-bromocADPR (a cell-permeable cADPR antagonist), ryanodine (an antagonist of ryanodine receptors), or nicotinamide (an ADP-ribosyl cyclase inhibitor). By in situ simultaneously fluorescent monitoring, Ca 2ϩ transient and nitric oxide (NO) levels in the intact coronary arterial endothelium preparation, 8-bromo-cADPR (30 M), ryanodine (50 M), and nicotinamide (6 mM) substantially attenuated BK (1 M)-induced increase in intracellular [Ca 2ϩ ] by 78%, 80%, and 74%, respectively, whereas these compounds significantly blocked BKinduced NO increase by about 80%, and inositol 1,4,5-trisphosphate receptor blockade with 2-aminethoxydiphenyl borate (50 M) only blunted BK-induced Ca 2ϩ -NO signaling by about 30%. With the use of cADPR-cycling assay, it was found that inhibition of ADP-ribosyl cyclase by nicotinamide substantially blocked BK-induced intracellular cADPR production. Furthermore, HPLC analysis showed that the conversion rate of ␤-nicotinamide guanine dinucleotide into cyclic GDP ribose dramatically increased by stimulation with BK, which was blockable by nicotinamide. However, U-73122, a phospholipase C inhibitor, had no effect on this BK-induced increase in ADP-ribosyl cyclase activity for cADPR production. In conclusion, these results suggest that cADPR importantly contributes to BK-and A-23187-induced NO production and vasodilator response in coronary arteries through its Ca 2ϩ signaling mechanism in CAECs.nucleotide; vasodilation; endothelium; endothelium-derived relaxing factor CYCLIC ADP RIBOSE (cADPR), endogenously generated from nicotinamide (Ni) adenine dinucleotide, has emerged as a novel intracellular Ca 2ϩ -mobilizing second messenger in a wide variety of mammalian cells. The actions of this signaling nucleotide are completely independent of the inositol 1,4,5-trisphosphate [Ins(1,4,5)P 3 ]-signaling pathway, but it exerts its action by targeting ryanodine (Ry) receptors (RyRs) (8,15,16,(31)(32)(33)44). Elevation of intracellular cADPR levels followed by Ca 2ϩ mobilizition and activation of Ca 2ϩ -dependent effects within cells has been found to be essential for versatile physiological processes, such as cell cycle regulation, cell proliferation, gene expression, egg fertilization, neurotransmitter release, muscle contraction, and nitric oxide signaling (10,29,55). Recent studies (17,35,36,52,55,57) in our laboratory and by others have reported that in va...

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Metabolism and Actions of ADP-Riboses in Coronary Arterial Smooth Muscle

Cited by 23 publications

References 8 publications

Pharmacological Modulation of Sarcoplasmic Reticulum Function in Smooth Muscle

Pharmacological Modulation of Sarcoplasmic Reticulum Function in Smooth Muscle

Modulation of store-operated Ca2+ entry by cyclic-ADP-ribose

Cyclic ADP ribose-mediated Ca²⁺signaling in mediating endothelial nitric oxide production in bovine coronary arteries

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Metabolism and Actions of ADP-Riboses in Coronary Arterial Smooth Muscle

Cited by 23 publications

References 8 publications

Pharmacological Modulation of Sarcoplasmic Reticulum Function in Smooth Muscle

Pharmacological Modulation of Sarcoplasmic Reticulum Function in Smooth Muscle

Modulation of store-operated Ca2+ entry by cyclic-ADP-ribose

Cyclic ADP ribose-mediated Ca2+signaling in mediating endothelial nitric oxide production in bovine coronary arteries

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Cyclic ADP ribose-mediated Ca²⁺signaling in mediating endothelial nitric oxide production in bovine coronary arteries