scholarly journals Monitoring ER/SR Calcium Release with the Targeted Ca2+ Sensor CatchER+

10.3791/55822 ◽  
2017 ◽  
Author(s):  
Florence N. Reddish ◽  
Cassandra L. Miller ◽  
Rakshya Gorkhali ◽  
Jenny J. Yang
Keyword(s):  
Calcium Release ◽  
Sr Calcium Release

Calcium-sensitivity of the SR calcium release channel in failing and nonfailing human myocardium

1999 ◽  
Vol 94 (3) ◽  
pp. 145-151 ◽  
Author(s):  
U. Schotten ◽  
C. Schumacher ◽  
V. Conrads ◽  
V. Braun ◽  
F. Schöndube ◽  
...  
Keyword(s):  
Calcium Release ◽  
Calcium Sensitivity ◽  
Human Myocardium ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Sr Calcium Release

scholarly journals Modulation of the Frequency of Spontaneous Sarcoplasmic Reticulum Ca2+ Release Events (Ca2+ Sparks) by Myoplasmic [Mg2+] in Frog Skeletal Muscle

1998 ◽  
Vol 111 (2) ◽  
pp. 207-224 ◽  
Author(s):  
Alain Lacampagne ◽  
Michael G. Klein ◽  
Martin F. Schneider
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Frog Skeletal Muscle ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Event Frequency ◽  
Open Time ◽  
Channel Opening ◽  
Sr Calcium Release

The modulation by internal free [Mg2+] of spontaneous calcium release events (Ca2+ “sparks”) from the sarcoplasmic reticulum (SR) was studied in depolarized notched frog skeletal muscle fibers using a laser scanning confocal microscope in line-scan mode (x vs. t). Over the range of [Mg2+] from 0.13 to 1.86 mM, decreasing the [Mg2+] induced an increase in the frequency of calcium release events in proportion to [Mg2+]−1.6. The change of event frequency was not due to changes in [Mg-ATP] or [ATP]. Analysis of individual SR calcium release event properties showed that the variation in event frequency induced by the change of [Mg2+] was not accompanied by any changes in the spatiotemporal spread (i.e., spatial half width or temporal half duration) of Ca2+ sparks. The increase in event frequency also had no effect on the distribution of event amplitudes. Finally, the rise time of calcium sparks was independent of the [Mg2+], indicating that the open time of the SR channel or channels underlying spontaneous calcium release events was not altered by [Mg2+] over the range tested. These results suggest that in resting skeletal fibers, [Mg2+] modulates the SR calcium release channel opening frequency by modifying the average closed time of the channel without altering the open time. A kinetic reaction scheme consistent with our results and those of bilayer and SR vesicle experiments indicates that physiological levels of resting Mg2+ may inhibit channel opening by occupying the site for calcium activation of the SR calcium release channel.

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

2006 ◽  
Vol 127 (2) ◽  
pp. 171-182 ◽  
Author(s):  
Haouaria Balghi ◽  
Stéphane Sebille ◽  
Bruno Constantin ◽  
Sylvie Patri ◽  
Vincent Thoreau ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Intracellular Signaling ◽  
Calcium Release ◽  
Ryanodine Receptors ◽  
Inhibitory Effect ◽  
Ip3 Receptors ◽  
High Potassium ◽  
Gi Protein ◽  
Kinetics Of ◽  
Sr Calcium Release

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.

scholarly journals Transient Mitochondrial Depolarizations Reflect Focal Sarcoplasmic Reticular Calcium Release in Single Rat Cardiomyocytes

1998 ◽  
Vol 142 (4) ◽  
pp. 975-988 ◽  
Author(s):  
Michael R. Duchen ◽  
Anne Leyssens ◽  
Martin Crompton
Keyword(s):  
Calcium Uptake ◽  
Calcium Release ◽  
Mitochondrial Calcium ◽  
Calcium Stores ◽  
Tight Coupling ◽  
Mitochondrial Potential ◽  
Rat Cardiomyocytes ◽  
Calcium Uniporter ◽  
Mitochondrial Calcium Uptake ◽  
Sr Calcium Release

Digital imaging of mitochondrial potential in single rat cardiomyocytes revealed transient depolarizations of mitochondria discretely localized within the cell, a phenomenon that we shall call “flicker.” These events were usually highly localized and could be restricted to single mitochondria, but they could also be more widely distributed within the cell. Contractile waves, either spontaneous or in response to depolarization with 50 mM K+, were associated with propagating waves of mitochondrial depolarization, suggesting that propagating calcium waves are associated with mitochondrial calcium uptake and consequent depolarization. Here we demonstrate that the mitochondrial flicker was directly related to the focal release of calcium from sarcoplasmic reticular (SR) calcium stores and consequent uptake of calcium by local mitochondria. Thus, the events were dramatically reduced by (a) depletion of SR calcium stores after long-term incubation in EGTA or thapsigargin (500 nM); (b) buffering intracellular calcium using BAPTA-AM loading; (c) blockade of SR calcium release with ryanodine (30 μM); and (d) blockade of mitochondrial calcium uptake by microinjection of diaminopentane pentammine cobalt (DAPPAC), a novel inhibitor of the mitochondrial calcium uniporter. These observations demonstrate that focal SR calcium release results in calcium microdomains sufficient to promote local mitochondrial calcium uptake, suggesting a tight coupling of calcium signaling between SR release sites and nearby mitochondria.

scholarly journals Mg 2+ Inhibits Cardiac SR Calcium Release and has Biphasic Effects on Calmodulin Binding to RyR2

2017 ◽  
Vol 112 (3) ◽  
pp. 255a
Author(s):  
Xiaoqiong Dong ◽  
Ivanita Stefanon ◽  
Rogerio F. Ribeiro ◽  
Mena Said ◽  
Robyn T. Rebbeck ◽  
...  
Keyword(s):  
Calcium Release ◽  
Calmodulin Binding ◽  
Sr Calcium Release
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