Capacitative calcium entry channels

Putney, James W.; McKay, Richard R.

doi:10.1002/(sici)1521-1878(199901)21:1<38::aid-bies5>3.0.co;2-s

Cited by 373 publications

(225 citation statements)

References 76 publications

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“…Recent data suggest that there might be a direct molecular interaction between components of the intracellular stores (such as the IP 3 receptor itself) and plasmalemmal TRP channels (see Putney & Mckay, 1999). However, there is the possibility that Ca 2+ released by CPA could activate phospholipid hydrolysis and produce second messenger(s) (Matkovich & Woodcock, 2000).…”

Section: British Journal Of Pharmacology Vol 133 (2)mentioning

confidence: 99%

“…Though a number of ion channels have been implicated in such in¯ux, the role of L-type voltage gated Ca 2+ channels in human ASM seems to be a relatively minor one. Attention has been recently drawn to store-operated Ca 2+ channels (SOC) which are activated upon emptying of IP 3 -dependent Ca 2+ stores (Putney & Mckay, 1999), and to a variety of channels directly activated by second messengers such as Ca 2+ , IP 3 , IP 4 , arachidonic acid and its metabolites (for review see Kiselyov & Muallem, 1999).…”

Section: Introductionmentioning

confidence: 99%

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Mechanisms of leukotriene D₄‐induced constriction in human small bronchioles

Snetkov

Hapgood

McVicker

et al. 2001

British J Pharmacology

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1 We examined the mechanisms underlying leukotriene D 4 -(LTD 4 ) induced constriction of human small (300 ± 500 mm i.d.) bronchioles, and the e ect of LTD 4 on ion currents and Ca 2+ transients in smooth muscle cells (SMC) isolated from these bronchioles. 2 LTD 4 caused a concentration-dependent bronchoconstriction with an EC 50 =0.58+0.05 nM (n=7) which was not easily reversible upon washout. This bronchoconstriction was entirely dependent on extracellular Ca 2+ . 3 Blockade of L-type Ca 2+ channels with nifedipine (10 mM) reduced LTD 4 response by 39+2% (n=8), whilst La 3+ , Gd 3+ and SK&F 96,365 abolished LTD 4 -induced bronchoconstriction completely and reversibly, suggesting the majority of Ca 2+ entry was via non-selective cation channels. 4 Antagonists of PI-PLC (U73,122 and ET-18-OCH 3 ), PLD (propranolol) and PKC (cheleretrine and Ro31-8220) were without any e ect on LTD 4 -induced bronchoconstriction, whilst the PC-PLC inhibitor D609 caused complete relaxation. Inhibition of protein tyrosine kinase with tyrphostin A23 (100 mM) caused about 50% relaxation, although the inactive analogue tyrphostin A1 was without e ect. 5 In freshly isolated SMC from human small bronchioles LTD 4 caused a slow increase of intracellular Ca 2+ concentration, with a consequent rise of the activity of large conductance Ca 2+ -dependent K + channels and the amplitude of depolarization-induced outward whole-cell current. Again, no e ect of LTD 4 could be observed in the absence of extracellular Ca 2+ . 6 We conclude that LTD 4 causes constriction of these small bronchioles primarily by activating Ca 2+ entry via non-voltage gated channels, possibly by a PC-PLC mediated pathway.

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Section: British Journal Of Pharmacology Vol 133 (2)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mechanisms of leukotriene D₄‐induced constriction in human small bronchioles

Snetkov

Hapgood

McVicker

et al. 2001

British J Pharmacology

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“…In the last case, store-operated Ca 2ϩ entry (SOCE) is triggered by depletion of SR Ca 2ϩ stores (6,41,42,49,55,56). We and others have shown that different transient receptor potential channel (TRPC) isoforms are expressed in ASM (6,58).…”

mentioning

confidence: 99%

Regulation of store-operated Ca²⁺entry by CD38 in human airway smooth muscle

Sieck¹,

White²,

Thompson³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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(11,15,20,26,38,39,46) or by plasma membrane Ca 2ϩ influx.TNF␣, a potent proinflammatory cytokine found in bronchoalveolar lavage fluid (12) and sputum (50) from asthmatics, has been implicated as a mediator in the pathophysiology of asthma (45, 51, 52) and chronic obstructive pulmonary disease (8, 16). Indeed, TNF␣ has been shown to enhance ASM contractility (13,43,47 (11,20,46) as well as via ryanodine receptor (RyR) channels (15, 26), the latter resulting from increased levels of the novel second messenger cyclic ADP ribose (cADPR) (27,39). cADPR, in turn, is synthesized and degraded by the bifunctional ectoenzyme CD38 via ADP ribosyl cyclase and cADPR hydrolase activities, respectively (22). Indeed, the CD38/cADPR pathway has been implicated in [Ca 2ϩ ] i regulation in ASM (39, 57) and intestinal (30, 31), uterine (7, 53), and vascular (17, 25) smooth muscles. Recent studies suggest that the CD38/cADPR signaling pathway contributes to TNF␣-induced augmentation of [Ca 2ϩ ] i responses in ASM (14). Such an effect is thought to result from an increase in cADPRinduced Ca 2ϩ mobilization from the SR. However, this does not explain the effect of TNF␣ on both peak and plateau responses. While it is likely that SR Ca 2ϩ release is augmented by TNF␣, whether Ca 2ϩ influx is also increased remains to be determined.Ca 2ϩ influx in ASM can occur through voltage-gated (59), receptor-operated (33), and/or store-operated channels (6). In the last case, store-operated Ca 2ϩ entry (SOCE) is triggered by depletion of SR Ca 2ϩ stores (6,41,42,49,55,56). We and others have shown that different transient receptor potential channel (TRPC) isoforms are expressed in ASM (6,58). In a recent study using human ASM, we further demonstrated that TNF␣ treatment increases SOCE (58). TNF␣ treatment also increases CD38 expression. Studies in other cell types suggest that CD38 itself can also regulate SOCE (10, 21). Whether altered CD38 expression contributes to TNF␣-induced changes in Ca 2ϩ influx is not known. In the present study, we hypothesized that the effects of TNF␣ treatment on CD38 expression and SOCE in human ASM cells are linked. Accordingly, we examined the effects of CD38 overexpression vs. knockdown of CD38 expression [via specific small interfering RNA (siRNA)] on TNF␣-induced enhancement of SOCE. METHODSHuman ASM cells. Human bronchi were obtained from discarded surgical specimens in accordance with procedures reviewed and approved (as well as deemed exempt from Human Subjects classification under 45CFR 46) by the Mayo Clinic Institutional Review Board. The techniques for isolation of ASM cells from bronchi have

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“…The mechanism for Ca 2ϩ entry has been studied extensively. In one mechanism, termed "store-operated Ca 2ϩ entry," the emptying of intracellular stores activates surface membrane Ca 2ϩ channels via either diffusible factors or a direct interaction between IP 3 receptors and surface Ca 2ϩ channels (55)(56)(57). These Ca 2ϩ -permeable channels on the cell surface are called store-operated channels (SOC).…”

Section: Role Of Trp In Plc-dependent Ca 2ϩ Influxmentioning

confidence: 99%

The Transient Receptor Potential Superfamily of Ion Channels

Huang

2004

Journal of the American Society of Nephrology

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Abstract. The transient receptor potential (TRP) superfamily of proteins is cation-selective ion channels with six predicted transmembrane segments and intracellularly localized amino and carboxyl termini. Members of the TRP superfamily are identified on the basis of amino acid sequence and structural similarity and are classified into TRPC, TRPV, TRPM, TRPP, TRPN, and TRPML subfamilies. TRP channels are widespread and have diverse functions, ranging from thermal, tactile, taste, osmolar, and fluid flow sensing to transepithelial Ca 2ϩ and Mg 2ϩ transport. Mutations of TRP proteins produce many renal diseases, including Mg 2ϩ wasting, hypocalcemia, and polycystic kidney diseases. This review focuses on recent advances in the understanding of their functions.The first transient receptor potential (TRP) protein was discovered in studies that examined Drosophila phototransduction (1). The photoreceptor cells of Drosophila exhibit sustained receptor potentials in response to continuous light exposure. The ionic basis for the sustained receptor potentials is influx of Ca 2ϩ from the extracellular space. Cosens and Manning (1) reported in 1969 that one group of mutant flies exhibits TRP upon continuous light exposure and named it trp, for transient receptor potential. The trp gene was cloned in 1989 (2) and subsequently shown to encode a Ca 2ϩ -permeable cation channel (3). Since then, many channels that bear sequence and structural similarities to the Drosophila TRP have been cloned from flies, worms, and mammals. Together, they form the TRP superfamily.Ion channels (e.g., voltage-gated K ϩ channels) are typically identified by their modes of activation and/or ion selectivity. Each family or superfamily of ion channels of similar activation and selectivity consists of multiple members of channel proteins with amino acid sequence homology. Unlike most ion channel families, the TRP superfamily of ion channels are identified on the basis of homology only. The mode of activation and selectivity for TRP channels are disparate. Some TRP channels are activated by ligands, whereas others are regulated by physical stimuli (e.g., heat) or yet-unknown mechanisms. All TRP channels are cation selective, but the selectivity ratio for Ca 2ϩ versus the monovalent cation Na ϩ (P Ca /P Na ) varies widely, ranging from Ͼ100:1, to 1 to 10:1, to Ͻ0.05:1. The lack of common identifying features has in part contributed to the confusing nomenclature of TRP channels in the literature.A recent consensus report proposed a unified nomenclature for the TRP superfamily (4). It classified TRP channels into TRPC, TRPV, and TRPM subfamilies. More recent classification has expanded TRP superfamily to include three additional, more distantly related subfamilies, TRPP, TRPML, and TRPN ( Figure 1). Structurally, all of these TRP channels have six predicted transmembrane (TM) segments and N-terminal and C-terminal cytoplasmic tails similar to topologies of voltagegated K ϩ , Na ϩ , and Ca 2ϩ channels; cyclic nucleotide-gated channels; and hyperpolarizati...

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Capacitative calcium entry channels

Cited by 373 publications

References 76 publications

Mechanisms of leukotriene D₄‐induced constriction in human small bronchioles

Mechanisms of leukotriene D₄‐induced constriction in human small bronchioles

Regulation of store-operated Ca²⁺entry by CD38 in human airway smooth muscle

The Transient Receptor Potential Superfamily of Ion Channels

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Capacitative calcium entry channels

Cited by 373 publications

References 76 publications

Mechanisms of leukotriene D4‐induced constriction in human small bronchioles

Mechanisms of leukotriene D4‐induced constriction in human small bronchioles

Regulation of store-operated Ca2+entry by CD38 in human airway smooth muscle

The Transient Receptor Potential Superfamily of Ion Channels

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Product

Resources

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Mechanisms of leukotriene D₄‐induced constriction in human small bronchioles

Mechanisms of leukotriene D₄‐induced constriction in human small bronchioles

Regulation of store-operated Ca²⁺entry by CD38 in human airway smooth muscle