Elementary and global aspects of calcium signalling.

Berridge, Michael J.

doi:10.1113/jphysiol.1997.sp021927

Cited by 1,018 publications

(929 citation statements)

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“…1C). In summary, the IP 3 -dependent elementary Ca 2+ release events in permeabilized atrial myocytes were distinctly different from Ca 2+ sparks and were reminiscent of Ca 2+ puffs typically observed in non-excitable tissue where IP 3 -dependent Ca 2+ signaling is predominant [79,80,82,84]. These data are consistent with the notion that IP 3 Rs provide a significantly smaller Ca 2+ release pathway compared to RyRs.…”

Section: Elementary Ip 3 -Induced Ca 2+ Release Events In Cardiac Myosupporting

confidence: 82%

“…Discrete, non-propagating elementary Ca 2+ release events have been characterized in a variety of excitable and non-excitable cell types (for reviews see [73,74]), for both RyRs ('Ca 2+ sparks'; [75][76][77][78]) and IP 3 Rs [70,79,80]. Ca 2+ sparks represent Ca 2+ release from a restricted number of clustered RyRs opening in concert [81].…”

Section: Elementary Ip 3 -Induced Ca 2+ Release Events In Cardiac Myomentioning

confidence: 99%

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Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes

Kockskämper

Zima

Roderick

et al. 2008

Journal of Molecular and Cellular Cardiology

173

149

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Inositol 1,4,5-trisphosphate (IP 3 ) is a ubiquitous intracellular messenger regulating diverse functions in almost all mammalian cell types. It is generated by membrane receptors that couple to phospholipase C (PLC), an enzyme which liberates IP 3 from phosphatidylinositol 4,5-bisphosphate (PIP 2 ). The major action of IP 3 , which is hydrophilic and thus translocates from the membrane into the cytoplasm, is to induce Ca 2+ release from endogenous stores through IP 3 receptors (IP 3 Rs). Cardiac excitation-contraction coupling relies largely on ryanodine receptor (RyR)-induced Ca 2+ release from the sarcoplasmic reticulum. Myocytes express a significantly larger number of RyRs compared to IP 3 Rs (∼100:1), and furthermore they experience substantial fluxes of Ca 2+ with each heartbeat. Therefore, the role of IP 3 and IP 3 -mediated Ca 2+ signaling in cardiac myocytes has long been enigmatic. Recent evidence, however, indicates that despite their paucity cardiac IP 3 Rs may play crucial roles in regulating diverse cardiac functions. Strategic localization of IP 3 Rs in cytoplasmic compartments and the nucleus enables them to participate in subsarcolemmal, bulk cytoplasmic and nuclear Ca 2+ signaling in embryonic stem cell-derived and neonatal cardiomyocytes, and in adult cardiac myocytes from the atria and ventricles. Intriguingly, expression of both IP 3 Rs and membrane receptors that couple to PLC/IP 3 signaling is altered in cardiac disease such as atrial fibrillation or heart failure, suggesting the involvement of IP 3 signaling in the pathology of these diseases. Thus, IP 3 exerts important physiological and pathological functions in the heart, ranging from the regulation of pacemaking, excitation-contraction and excitation-transcription coupling to the initiation and/or progression of arrhythmias, hypertrophy and heart failure. KeywordsInositol 1,4,5-trisphosphate; Cardiac myocyte; Calcium; Inotropy; Arrhythmias; Nucleus; Hypertrophy © 2008 Elsevier Inc. All rights reserved. * Corresponding author. E-mail address: jens.kockskaemper@meduni-graz.at (J. Kockskämper).. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript The discovery of IP 3A quarter of a century ago it was shown that D-myo inositol 1,4,5-trisphosphate (IP 3 ) releases Ca 2+ from a non-mitochondrial internal Ca 2+ store [1]. Since this hallmark discovery, IP 3 has emerged as a ubiquitous intracellular messenger, releasing Ca 2+ from stores through activation of IP 3 receptors (IP 3 Rs) in almost all eukaryotic cells. The major IP 3 -sensitive intracellular Ca 2+ store is the endoplasmic reticulum. However, IP 3 has also been shown to release Ca 2+ stored in other compartments, such as the Golgi and the nuclear envelope [2]. In addition, IP 3 Rs are present on the plasma membrane of some cell types, where they can gate Ca 2+ influx [3]. A crucial role for IP 3 -dependent Ca 2+ release has been demonstrated in many mammalian cell types, ranging from tiny platelets, where it initiates blood clottin...

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Section: Elementary Ip 3 -Induced Ca 2+ Release Events In Cardiac Myosupporting

confidence: 82%

Section: Elementary Ip 3 -Induced Ca 2+ Release Events In Cardiac Myomentioning

confidence: 99%

Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes

Kockskämper

Zima

Roderick

et al. 2008

Journal of Molecular and Cellular Cardiology

173

149

View full text Add to dashboard Cite

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“…In the immature Xenopus oocyte, for example, IP 3 Rs occur in clusters of 10-100 with inter-cluster spacing on the order of a few microns (8). Localized Ca 2+ elevations due to the activation of an individual IP 3 -sensitive Ca 2+ release sites are referred to as 'Ca 2+ puffs' (44; 45) and under some conditions this organization of Ca 2+ release sites reveals itself in cauliflower-like wave fronts (46).…”

Section: Introductionmentioning

confidence: 99%

A bidomain threshold model of propagating calcium waves

2007

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We present a bidomain fire-diffuse-fire model that facilitates mathematical analysis of propagating waves of elevated intracellular calcium (Ca 2+ ) in living cells. Modelling Ca 2+ release as a threshold process allows the explicit construction of travelling wave solutions to probe the dependence of Ca 2+ wave speed on physiologically important parameters such as the threshold for Ca 2+ release from the endoplasmic reticulum (ER) to the cytosol, the rate of Ca 2+ resequestration from the cytosol to the ER, and the total [Ca 2+ ] (cytosolic plus ER). Interestingly, linear stability analysis of the bidomain fire-diffuse-fire model predicts the onset of dynamic wave instabilities leading to the emergence of Ca 2+ waves that propagate in a back-and-forth manner. Numerical simulations are used to confirm the presence of these so-called 'tango waves' and the dependence of Ca 2+ wave speed on the total [Ca 2+ ].

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“…Fluctuations in cytosolic Ca# + signalling in the form of oscillations or ' spiking ' have been observed in a wide variety of cell when receptors activating the phosphoinositide signalling cascade are stimulated. There are a variety of oscillatory patterns which are determined by such factors as cell specificity, agonist type and concentration, as well as extracellular Ca# + concentration (see [29,30]). In L-cells, the pattern of oscillations can be categorized as being sinusoidal, as opposed to baseline spiking, because oscillations occur over and above an elevated plateau Ca# + level [31].…”

Section: Discussionmentioning

confidence: 99%

Enhanced purinoceptor-mediated Ca2+ signalling in L-fibroblasts overexpressing type 1 inositol 1,4,5-trisphosphate receptors

Davis

Challiss

Nahorski

1999

Biochemical Journal

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Mouse L-fibroblast cells stably transfected with either type 1 Ins(1,4,5)P $ receptor (InsP $ R) cDNA (L15) or the vector control (Lvec) have been used to investigate the functional consequences of increased InsP $ R density on receptor-mediated Ca# + signalling. L15 cells express approx. 8-fold higher levels of the type 1 InsP $ R compared with Lvec cells, which endogenously express essentially only the type 1 InsP $ R protein. Stimulation of Lvec and L15 cells with UTP or ATP increased cytosolic Ca# + concentration to a greater extent in L15 cells at all agonist concentrations. UTP and ATP were equipotent, suggestive of the presence of endogenous cell-surface metabotropic P2Y # -purinoceptors. In both cell clones the purinoceptors were coupled via pertussis-toxin-insensitive Gprotein(s) to phospholipase C activation, resulting in similar concentration-dependent accumulations of InsP $ . Single-cell microfluorimetry revealed that overexpression of InsP $ Rs reduced the threshold for purinoceptor-mediated Ca# + signalling. L-

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Elementary and global aspects of calcium signalling.

Cited by 1,018 publications

References 118 publications

Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes

Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes

A bidomain threshold model of propagating calcium waves

Enhanced purinoceptor-mediated Ca2+ signalling in L-fibroblasts overexpressing type 1 inositol 1,4,5-trisphosphate receptors

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