Nicotinic Acid Adenine Dinucleotide Phosphate Mediates Ca
            <sup>2+</sup>
            Signals and Contraction in Arterial Smooth Muscle via a Two-Pool Mechanism

Boittin, François-Xavier; Galione, Antony; Evans, A. Mark

doi:10.1161/01.res.0000047507.22487.85

Cited by 107 publications

(149 citation statements)

References 37 publications

Supporting

Mentioning

124

Contrasting

Order By: Relevance

“…In paired cells, intracellular dialysis of NAADP-free pipette solution had little or no effect (n ϭ 17; not shown). Our findings are consistent with the view that the events leading up to the initiation of global Ca 2ϩ waves by NAADP are complex, in that there is a highly localized release of Ca 2ϩ , which precedes the global Ca 2ϩ waves and the associated contractile response (13). In general, this initial localized Ca 2ϩ release event appears as 1) a uniform increase in Fura-2 fluorescence ratio around the entire perimeter of the cell ( Fig.…”

Section: Resultssupporting

confidence: 91%

“…Consistent with this proposal, the enzymes for the synthesis and metabolism of NAADP (5,6) and cyclic ADP-ribose (7) have been shown to be associated with smooth muscle in addition to other cell types. In smooth muscle, cyclic ADP-ribose may mobilize Ca 2ϩ from the SR by activating RyRs (8 -12), whereas our studies on arterial smooth muscle (13) are consistent with the idea that NAADP mobilizes Ca 2ϩ from an undefined store that may be coupled to the SR (14 -16). Briefly, we have demonstrated that NAADP triggers spatially restricted Ca 2ϩ bursts in arterial smooth muscle, which subsequently elicit a global Ca 2ϩ wave and muscle contraction by CICR via RyRs (13).…”

supporting

confidence: 76%

“…1A and 2A, panel ii). These localized Ca 2ϩ signals initiated by NAADP have been named "Ca 2ϩ bursts" (13) and either decline back to basal levels or trigger a global Ca 2ϩ wave (Fig. 1A).…”

Section: Resultsmentioning

confidence: 99%

“…Intracellular Dialysis of NAADP and IP 3 -Ca 2ϩ -mobilizing second messengers were applied intracellularly in the whole cell configuration of the patch clamp technique, and in current clamp mode (I ϭ 0) as described previously (13). The pipette solution contained (mM): 140 KCl, 10 Hepes, 1 MgCl 2 , and 5 M Fura-2, pH 7.4.…”

Section: Methodsmentioning

confidence: 99%

See 3 more Smart Citations

Lysosome-Sarcoplasmic Reticulum Junctions

Kinnear

Boittin

Thomas

et al. 2004

Journal of Biological Chemistry

Self Cite

182

120

View full text Add to dashboard Cite

Previous studies on pulmonary arterial smooth muscle cells have shown that nicotinic acid adenine dinucleotide phosphate (NAADP) evokes highly localized intracellular Ca 2؉ signals by mobilizing thapsigargininsensitive stores. Such localized Ca 2؉ signals may initiate global Ca 2؉ waves and contraction of the myocytes through the recruitment of ryanodine receptors on the sarcoplasmic reticulum via Ca 2؉ -induced Ca 2؉ release. Here we show that NAADP evokes localized Ca 2؉ signals by mobilizing a bafilomycin A1-sensitive, lysosome-related Ca 2؉ store. These lysosomal stores facilitate this process by co-localizing with a portion of the sarcoplasmic reticulum expressing ryanodine receptors to comprise a highly specialized trigger zone for NAADPdependent Ca 2؉ signaling by the vasoconstrictor hormone, endothelin-1. These findings further advance our understanding of how the spatial organization of discrete, organellar Ca 2؉ stores may underpin the generation of differential Ca 2؉ signaling patterns by different Ca 2؉ -mobilizing messengers.

show abstract

Section: Resultssupporting

confidence: 91%

supporting

confidence: 76%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Lysosome-Sarcoplasmic Reticulum Junctions

Kinnear

Boittin

Thomas

et al. 2004

Journal of Biological Chemistry

Self Cite

182

120

View full text Add to dashboard Cite

show abstract

“…These enzymes also possess a transglycosidation (base-exchange) activity capable of exchanging the nicotinamide moiety of NAD(P) with nicotinic acid or other nucleophiles. In the presence of nicotinic acid and NADP, the base-exhange reaction of the ADP-ribosyl cyclase family is responsible for generating nicotinic acid adenine dinucleotide phosphate (NAADP), another compound capable of regulating calcium release from intracellular stores in a variety of cell types, including those of some smooth muscles (57)(58)(59)(60)(61)(62).…”

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

View full text Add to dashboard Cite

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...

show abstract