Subtype identification and functional properties of inositol 1,4,5-trisphosphate receptors in heart and aorta

Tovey, Stephen C.; Dyer, Jeanette L.; Godfrey, Rita E.; Khan, Shahla Zafar; Bilmen, Jonathan G.; Mezna, Mokdad; Michelangeli, Francesco

doi:10.1006/phrs.2000.0733

Cited by 12 publications

(5 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…More importantly, tetracaine appeared to mediate its action by altering Ca 2ϩ signaling and Ca 2ϩ sensitization. In other studies, tetracaine has been suggested to block IP 3 -mediated Ca 2ϩ release at high concentrations (1 mM) (36,51). However, we found that 50 M tetracaine does not affect Ca 2ϩ release in response to IP 3 .…”

Section: Discussioncontrasting

confidence: 78%

The contribution of inositol 1,4,5-trisphosphate and ryanodine receptors to agonist-induced Ca²⁺ signaling of airway smooth muscle cells

Bai

Edelmann²,

Sanderson³

2009

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

The relative contribution of inositol 1,4,5-trisphosphate (IP(3)) receptors (IP(3)Rs) and ryanodine receptors (RyRs) to agonist-induced Ca(2+) signaling in mouse airway smooth muscle cells (SMCs) was investigated in lung slices with phase-contrast or laser scanning microscopy. At room temperature (RT), methacholine (MCh) or 5-hydroxytryptamine (5-HT) induced Ca(2+) oscillations and an associated contraction in small airway SMCs. The subsequent exposure to an IP(3)R antagonist, 2-aminoethoxydiphenyl borate (2-APB), inhibited the Ca(2+) oscillations and induced airway relaxation in a concentration-dependent manner. 2-APB also inhibited Ca(2+) waves generated by the photolytic release of IP(3). However, the RyR antagonist ryanodine had no significant effect, at any concentration, on airway contraction or agonist- or IP(3)-induced Ca(2+) oscillations or Ca(2+) wave propagation. By contrast, a second RyR antagonist, tetracaine, relaxed agonist-contracted airways and inhibited agonist-induced Ca(2+) oscillations in a concentration-dependent manner. However, tetracaine did not affect IP(3)-induced Ca(2+) release or wave propagation nor the Ca(2+) content of SMC Ca(2+) stores as evaluated by Ca(2+)-release induced by caffeine. Conversely, both ryanodine and tetracaine completely blocked agonist-independent slow Ca(2+) oscillations induced by KCl. The inhibitory effects of 2-APB and absence of an effect of ryanodine on MCh-induced airway contraction or Ca(2+) oscillations of SMCs were also observed at 37 degrees C. In Ca(2+)-permeable SMCs, tetracaine inhibited agonist-induced contraction without affecting intracellular Ca(2+) levels indicating that relaxation also resulted from a reduction in Ca(2+) sensitivity. These results indicate that agonist-induced Ca(2+) oscillations in mouse small airway SMCs are primary mediated via IP(3)Rs and that tetracaine induces relaxation by both decreasing Ca(2+) sensitivity and inhibiting agonist-induced Ca(2+) oscillations via an IP(3)-dependent mechanism.

show abstract

Section: Discussioncontrasting

confidence: 78%

The contribution of inositol 1,4,5-trisphosphate and ryanodine receptors to agonist-induced Ca²⁺ signaling of airway smooth muscle cells

Bai

Edelmann²,

Sanderson³

2009

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

show abstract

“…These results suggest that Ca 2ϩ released from IP 3 Rs following submaximal agonist stimulation may open neighboring RyRs and then induce further Ca 2ϩ release from the SR (CICR), which amplifies agonist-induced increase in [Ca 2ϩ ] i and contraction in PASMCs. Since it has been reported that RyR antagonists may inhibit IP 3 Rs directly or indirectly (Vites and Pappano, 1992;Yamazawa et al, 1992;Iino et al, 1994;Tovey et al, 2000;Zimmermann, 2000;Flynn et al, 2001), one might argue that the inhibition of IP 3 Rs could account for the effects of the RyR antagonists on noradrenaline-induced Ca 2ϩ release and contraction in PASMCs. However, our data and previous reports indicate that this may not be the case in pulmonary artery (vascular) SMCS.…”

Section: Discussionmentioning

confidence: 99%

“…Since RyR antagonists have been reported to inhibit IP 3 Rs directly or indirectly (Vites and Pappano, 1992;Yamazawa et al, 1992;Iino et al, 1994;Tovey et al, 2000;Zimmermann, 2000;Flynn et al, 2001), we sought to examine the specificity of the RyR antagonists on neurotransmitter-induced Ca 2ϩ release in cultured human PASMCs, since these cells lack functional expression of RyRs (Fig. 3).…”

Section: Ryanodine Receptors Amplify Submaximal Neurotransmitterinduced Ca 2ϩ Release and Contraction In Pasmcsmentioning

confidence: 99%

Type-3 Ryanodine Receptors Mediate Hypoxia-, but Not Neurotransmitter-induced Calcium Release and Contraction in Pulmonary Artery Smooth Muscle Cells

Zheng

Wang

Rathore

et al. 2005

The Journal of General Physiology

121

View full text Add to dashboard Cite

In this study we examined the expression of RyR subtypes and the role of RyRs in neurotransmitter- and hypoxia-induced Ca2+ release and contraction in pulmonary artery smooth muscle cells (PASMCs). Under perforated patch clamp conditions, maximal activation of RyRs with caffeine or inositol triphosphate receptors (IP3Rs) with noradrenaline induced equivalent increases in [Ca2+]i and Ca2+-activated Cl− currents in freshly isolated rat PASMCs. Following maximal IP3-induced Ca2+ release, neither caffeine nor chloro-m-cresol induced a response, whereas prior application of caffeine or chloro-m-cresol blocked IP3-induced Ca2+ release. In cultured human PASMCs, which lack functional expression of RyRs, caffeine failed to affect ATP-induced increases in [Ca2+]i in the presence and absence of extracellular Ca2+. The RyR antagonists ruthenium red, ryanodine, tetracaine, and dantrolene greatly inhibited submaximal noradrenaline– and hypoxia-induced Ca2+ release and contraction in freshly isolated rat PASMCs, but did not affect ATP-induced Ca2+ release in cultured human PASMCs. Real-time quantitative RT-PCR and immunofluorescence staining indicated similar expression of all three RyR subtypes (RyR1, RyR2, and RyR3) in freshly isolated rat PASMCs. In freshly isolated PASMCs from RyR3 knockout (RyR3−/−) mice, hypoxia-induced, but not submaximal noradrenaline–induced, Ca2+ release and contraction were significantly reduced. Ruthenium red and tetracaine can further inhibit hypoxic increase in [Ca2+]i in RyR3−/− mouse PASMCs. Collectively, our data suggest that (a) RyRs play an important role in submaximal noradrenaline– and hypoxia-induced Ca2+ release and contraction; (b) all three subtype RyRs are expressed; and (c) RyR3 gene knockout significantly inhibits hypoxia-, but not submaximal noradrenaline–induced Ca2+ and contractile responses in PASMCs.

show abstract

“…64 All incubations and experiments were carried out at room temperature (23.51C). Imaging was performed by transferring a single glass coverslip into a perfusion chamber mounted on a Zeiss 135 inverted microscope equipped with a 100 W mercury arc lamp (RatioArc; Atto Instruments).…”

Section: Calcium Imagingmentioning

confidence: 99%

Anandamide-induced cell death in primary neuronal cultures: role of calpain and caspase pathways

et al. 2004

View full text Add to dashboard Cite

Anandamide (arachidonoylethanolamide or AEA) is an endocannabinoid that acts at vanilloid (VR1) as well as at cannabinoid (CB1/CB2) and NMDA receptors. Here, we show that AEA, in a dose-dependent manner, causes cell death in cultured rat cortical neurons and cerebellar granule cells. Inhibition of CB1, CB2, VR1 or NMDA receptors by selective antagonists did not reduce AEA neurotoxicity. Anandamideinduced neuronal cell loss was associated with increased intracellular Ca 2 þ , nuclear condensation and fragmentation, decreases in mitochondrial membrane potential, translocation of cytochrome c, and upregulation of caspase-3-like activity. However, caspase-3, caspase-8 or caspase-9 inhibitors, or blockade of protein synthesis by cycloheximide did not alter anandamide-related cell death. Moreover, AEA caused cell death in caspase-3-deficient MCF-7 cell line and showed similar cytotoxic effects in caspase-9 dominantnegative, caspase-8 dominant-negative or mock-transfected SH-SY5Y neuroblastoma cells. Anandamide upregulated calpain activity in cortical neurons, as revealed by a-spectrin cleavage, which was attenuated by the calpain inhibitor calpastatin. Calpain inhibition significantly limited anandamide-induced neuronal loss and associated cytochrome c release. These data indicate that AEA neurotoxicity appears not to be mediated by CB1, CB2, VR1 or NMDA receptors and suggest that calpain activation, rather than intrinsic or extrinsic caspase pathways, may play a critical role in anandamide-induced cell death.

show abstract

Subtype identification and functional properties of inositol 1,4,5-trisphosphate receptors in heart and aorta

Cited by 12 publications

References 39 publications

The contribution of inositol 1,4,5-trisphosphate and ryanodine receptors to agonist-induced Ca²⁺ signaling of airway smooth muscle cells

The contribution of inositol 1,4,5-trisphosphate and ryanodine receptors to agonist-induced Ca²⁺ signaling of airway smooth muscle cells

Type-3 Ryanodine Receptors Mediate Hypoxia-, but Not Neurotransmitter-induced Calcium Release and Contraction in Pulmonary Artery Smooth Muscle Cells

Anandamide-induced cell death in primary neuronal cultures: role of calpain and caspase pathways

Contact Info

Product

Resources

About

Subtype identification and functional properties of inositol 1,4,5-trisphosphate receptors in heart and aorta

Cited by 12 publications

References 39 publications

The contribution of inositol 1,4,5-trisphosphate and ryanodine receptors to agonist-induced Ca2+ signaling of airway smooth muscle cells

The contribution of inositol 1,4,5-trisphosphate and ryanodine receptors to agonist-induced Ca2+ signaling of airway smooth muscle cells

Type-3 Ryanodine Receptors Mediate Hypoxia-, but Not Neurotransmitter-induced Calcium Release and Contraction in Pulmonary Artery Smooth Muscle Cells

Anandamide-induced cell death in primary neuronal cultures: role of calpain and caspase pathways

Contact Info

Product

Resources

About

The contribution of inositol 1,4,5-trisphosphate and ryanodine receptors to agonist-induced Ca²⁺ signaling of airway smooth muscle cells

The contribution of inositol 1,4,5-trisphosphate and ryanodine receptors to agonist-induced Ca²⁺ signaling of airway smooth muscle cells