Inositol 1,4,5-trisphosphate receptor isoforms show similar Ca2+release kinetics

Dyer, Jeanette L.; Michelangeli, Francesco

doi:10.1054/ceca.2001.0231

Cited by 8 publications

(3 citation statements)

References 22 publications

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“…Similarly, NOmediated ER Ca 2ϩ release via RyRs is considered to be an important pathological step in interleukin (IL)-1␤-induced pyrogenic effects (485). 133,420). Similarly, in many nonexcitable cells, such as astrocytes, hepatocytes, exocrine cells, and vascular epithelium, the maximal IICR was observed at InsP 3 concentrations not exceeding 5-10 M (285); however, very high doses of InsP 3 (up to 100 M) were required to trigger maximal response in pancreatic acinar cells (681).…”

Section: Endogenous Cicr Modulatorsmentioning

confidence: 99%

Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons

Verkhratsky¹

2005

Physiological Reviews

667

602

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The endoplasmic reticulum (ER) is the largest single intracellular organelle, which is present in all types of nerve cells. The ER is an interconnected, internally continuous system of tubules and cisterns, which extends from the nuclear envelope to axons and presynaptic terminals, as well as to dendrites and dendritic spines. Ca(2+) release channels and Ca(2+) pumps residing in the ER membrane provide for its excitability. Regulated ER Ca(2+) release controls many neuronal functions, from plasmalemmal excitability to synaptic plasticity. Enzymatic cascades dependent on the Ca(2+) concentration in the ER lumen integrate rapid Ca(2+) signaling with long-lasting adaptive responses through modifications in protein synthesis and processing. Disruptions of ER Ca(2+) homeostasis are critically involved in various forms of neuropathology.

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Section: Endogenous Cicr Modulatorsmentioning

confidence: 99%

Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons

Verkhratsky¹

2005

Physiological Reviews

667

602

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“…The various types of InsP 3 Rs are not only differently regulated by Ca 2+ , they also bind InsP 3 with different affinities. These differences influence the potency of InsP 3 to release Ca 2+ (Missiaen et al, 1998; Wojcikiewicz and Luo, 1998; Miyakawa et al, 1999; Dyer and Michelangeli, 2001). In our model, these differences are reflected by distinct half‐saturation constants for InsP 3 R activation by InsP 3 .…”

Section: Mathematical Modelmentioning

confidence: 99%

Modelling the effect of specific inositol 1,4,5‐trisphosphate receptor isoforms on cellular Ca²⁺ signals

Dupont

Combettes

2006

Biology of the Cell

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Background information. Oscillations of cytosolic Ca2+ are well-known to rely on the regulatory properties of the InsP 3 R (inositol 1,4,5-trisphosphate receptor). imply different dynamical behaviours when these receptors are present in a cellular environment. We therefore describe by a specific phenomenological model the three main types of curves that have been reported: (i) the classical bell-shaped curve, (ii) the bell-shaped curve that is shifted towards higher Ca 2+ concentrations when InsP 3 is increased, and (iii) a monotonous increasing function of cytosolic Ca 2+ .Results. We show that, although these types of curves can be ascribed to slight differences in the channel regulation by Ca 2+ and InsP 3 , they can indicate important variations as to the receptor role in cellular Ca 2+ control. Thus the receptor associated with the classical bell-shaped curve appears to be the most robust Ca 2+ oscillator. If the steady-state curve is supposed to be a monotonous increasing function of cytosolic Ca 2+ , the modelled receptor cannot sustain Ca 2+ oscillations in the absence of Ca 2+ exchanges with the extracellular medium. When the bellshaped curve is shifted towards higher Ca 2+ concentrations with increasing InsP 3 levels, the model predicts that the receptor is less robust to changes in density; this receptor, however, provides a finer control of the steady-state level of Ca 2+ when varying the InsP 3 concentration. Conclusions.Our model allows us to propose an explanation for the experimental observations about the effect of selectively expressing or down-regulating InsP 3 R isoforms, as well as to make theoretical predictions.

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“…Nevertheless, the inositol 1,4,5trisphosphate receptor (IP3R) family of Ca 2+ release channels, which play a key role in Ca 2+ signaling in many other mammalian cells (Berridge, 1993;Blondel et al, 1994;Bootman et al, 1995;Furuichi and Mikoshiba, 1995), is thought to play a role in muscle cells. The process of IP3-induced Ca 2+ release has been well documented in smooth muscle cells (Miyakawa et al, 1999;Patel et al, 1999;Dyer and Michelangeli, 2001). More controversial, however, is the idea that IP3 may modulate EC coupling in cardiac muscle (Lipp et al, 2000), which also remains poorly understood in skeletal muscle cells.…”

Section: Introductionmentioning

confidence: 99%

Mini-dystrophin Expression Down-regulates Overactivation of G Protein–mediated IP3 Signaling Pathway in Dystrophin-deficient Muscle Cells

Balghi

Sebille

Constantin

et al. 2006

The Journal of General Physiology

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We present here evidence for the enhancement of an inositol 1,4,5-trisphosphate (IP3) mediated calcium signaling pathway in myotubes from dystrophin-deficient cell lines (SolC1(−)) as compared to a cell line from the same origin but transfected with mini-dystrophin (SolD(+)). With confocal microscopy, we demonstrated that calcium rise, induced by the perifusion of a solution containing a high potassium concentration, was higher in SolC1(−) than in SolD(+) myotubes. The analysis of amplitude and kinetics of the calcium increase in SolC1(−) and in SolD(+) myotubes during the exposure with SR Ca2+ channel inhibitors (ryanodine and 2-APB) suggested the presence of two mechanisms of SR calcium release: (1) a fast SR calcium release that depended on ryanodine receptors and (2) a slow SR calcium release mediated by IP3 receptors. Detection analyses of mRNAs (reverse transcriptase [RT]-PCR) and proteins (Western blot and immunolocalization) demonstrated the presence of the three known isoforms of IP3 receptors in both SolC1(−) and SolD(+) myotubes. Furthermore, analysis of the kinetics of the rise in calcium revealed that the slow IP3-dependent release may be increased in the SolC1(−) as compared to the SolD(+), suggesting an inhibitory effect of mini-dystrophin in this signaling pathway. Upon incubation with pertussis toxin (PTX), an inhibitory effect similar to that of the IP3R inhibitor (2-APB) was observed on K+-evoked calcium release. This result suggests the involvement of a Gi protein upstream of the IP3 pathway in these stimulation conditions. A hypothetical model is depicted in which both Gi protein and IP3 production could be involved in K+-evoked calcium release as well as a possible interaction with mini-dystrophin. Our findings demonstrate the existence of a potential relationship between mini-dystrophin and SR calcium release as well as a regulatory role of mini-dystrophin on intracellular signaling.

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Inositol 1,4,5-trisphosphate receptor isoforms show similar Ca2+release kinetics

Cited by 8 publications

References 22 publications

Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons

Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons

Modelling the effect of specific inositol 1,4,5‐trisphosphate receptor isoforms on cellular Ca²⁺ signals

Mini-dystrophin Expression Down-regulates Overactivation of G Protein–mediated IP3 Signaling Pathway in Dystrophin-deficient Muscle Cells

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Inositol 1,4,5-trisphosphate receptor isoforms show similar Ca2+release kinetics

Cited by 8 publications

References 22 publications

Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons

Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons

Modelling the effect of specific inositol 1,4,5‐trisphosphate receptor isoforms on cellular Ca2+ signals

Mini-dystrophin Expression Down-regulates Overactivation of G Protein–mediated IP3 Signaling Pathway in Dystrophin-deficient Muscle Cells

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Modelling the effect of specific inositol 1,4,5‐trisphosphate receptor isoforms on cellular Ca²⁺ signals