Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum

Fabiato, A

doi:10.1152/ajpcell.1983.245.1.c1

Cited by 1,757 publications

(877 citation statements)

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“…Intracellular Ca 2+ mishandling critically underlies the mechanical defects in failing myocardium 1. A tight junction between specialized domains of the sarcoplasmic reticulum (SR) and sarcolemmal transverse tubules (t‐tubules), called calcium release units , determines intracellular Ca 2+ homeostasis and consequent cardiomyocyte contractility 2, 3, 4. Ultrastructural rearrangements to SR and t‐tubule networks represent a major feature in cases of heart failure 5, 6, 7.…”

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confidence: 99%

REEP5 (Receptor Accessory Protein 5) Acts as a Sarcoplasmic Reticulum Membrane Sculptor to Modulate Cardiac Function

Yao

Xie

et al. 2018

JAHA

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BackgroundHeart failure is a complex syndrome characterized by cardiac contractile impairment with high mortality. Defective intracellular Ca2+ homeostasis is the central cause under this scenario and tightly links to ultrastructural rearrangements of sarcolemmal transverse tubules and the sarcoplasmic reticulum (SR); however, the modulators of the SR architecture remain unknown. The SR has been thought to be a specialized endoplasmic reticulum membrane system. Receptor accessory proteins (REEPs)/DP1/Yop1p are responsible for shaping high‐curvature endoplasmic reticulum tubules. This study aimed to determine the role of REEPs in SR membrane shaping and thus cardiac function.Methods and ResultsWe identified REEP5 (receptor accessory protein 5) as more highly expressed than other REEP members in adult rat ventricular myocardium, and it was downregulated in the failing hearts. Targeted inactivation of REEP5 in rats specially deformed the cardiac SR membrane without affecting transverse tubules, and this was visualized by focused ion beam scanning electron microscopy–based 3‐dimensional reconstruction. Accordingly, simultaneous recordings of depolarization‐induced Ca2+ currents and Ca2+ transients in REEP5‐null cardiomyocytes revealed normal L‐type Ca2+ channel currents but a depressed SR Ca2+ release. Consequently, the excitation–contraction coupling gain of cardiomyocytes and consequent cardiac contractility were compromised. REEP5 deficiency did not alter the expression of major proteins involved in Ca2+ handling in the heart.Conclusions REEP5 modulates cardiac function by shaping the SR. REEP5 defect deforms the SR architecture to depress cardiac contractility. REEP5‐dependent SR shaping might have potential as a therapeutic target for heart failure.

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confidence: 99%

REEP5 (Receptor Accessory Protein 5) Acts as a Sarcoplasmic Reticulum Membrane Sculptor to Modulate Cardiac Function

Yao

Xie

et al. 2018

JAHA

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“…Intracellular calcium handling is regulated by the Na + /Ca 2+ exchanger, L-type channel, sarcoplasmic reticulum (SR), ryanodine channel (RYR2), SR Ca 2+ -ATPase pump (SERCA2), phospholamban (PLB), and myofilament Ca 2+ affinity (10). Thus, any alteration in the expression of Ca 2+ -related genes could lead to abnormal Ca 2+ homeostasis and hence contractile dysfunction in cardiac tissue from food-restricted rats.…”

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confidence: 99%

Down-regulation of the cardiac sarcoplasmic reticulum ryanodine channel in severely food-restricted rats

Vizotto

Carvalho

Sugizaki

et al. 2007

Braz J Med Biol Res

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We have shown that myocardial dysfunction induced by food restriction is related to calcium handling. Although cardiac function is depressed in food-restricted animals, there is limited information about the molecular mechanisms that lead to this abnormality. The present study evaluated the effects of food restriction on calcium cycling, focusing on sarcoplasmic Ca 2+ -ATPase (SERCA2), phospholamban (PLB), and ryanodine channel (RYR2) mRNA expressions in rat myocardium. Male Wistar-Kyoto rats, 60 days old, were submitted to ad libitum feeding (control rats) or 50% diet restriction for 90 days. The levels of left ventricle SERCA2, PLB, and RYR2 were measured using semi-quantitative RT-PCR. Body and ventricular weights were reduced in 50% food-restricted animals. RYR2 mRNA was significantly decreased in the left ventricle of the foodrestricted group (control = 5.92 ± 0.48 vs food-restricted group = 4.84 ± 0.33, P < 0.01). The levels of SERCA2 and PLB mRNA were similar between groups (control = 8.38 ± 0.44 vs food-restricted group = 7.96 ± 0.45, and control = 1.52 ± 0.06 vs food-restricted group = 1.53 ± 0.10, respectively). Down-regulation of RYR2 mRNA expressions suggests that chronic food restriction promotes abnormalities in sarcoplasmic reticulum Ca 2+ release. Key wordsFood restriction induces beneficial health effects such as increased longevity and retards or prevents a broad spectrum of agerelated pathophysiological changes such as loss of skeletal muscle mass, diabetes mellitus, hypertension, and cancer (1-3). Recent research from our laboratory has shown that 50% food restriction promotes left ventricular dysfunction and increases contraction and relaxation times in isolated papillary muscle of both young Wistar-Kyoto normotensive and spontaneously hypertensive rats (4-7). Sugizaki et al. (7) observed that myocardial dysfunction in food-restricted rats is related to calcium handling. However, these investigators were unable to identify calcium handling site abnormalities.Few studies have analyzed the molecular

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“…The results presented here, on both fresh tissue and isolated cells, suggest that Ca 2+ is released from the stores independently of extracellular Ca 2+ . This is an interesting finding, as all muscular systems of invertebrates need external Ca 2+ for contraction, a feature shared with vertebrate cardiac muscles (Fabiato, 1983;Inoue et al, 1994). In isolated iridophores both KCl and muscarine evoked vigorous Ca 2+ transients, suggesting that calcium-induced-calcium-release may not be the only mechanism for triggering Ca 2+ release.…”

Section: Cytoplasmic Ca 2+ Measurementsmentioning

confidence: 92%

The role of muscarinic receptors and intracellular Ca2+ in the spectral reflectivity changes of squid iridophores

Mäthger

Collins

Lima

2004

Journal of Experimental Biology

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SUMMARYIn this paper we describe changes in spectral reflectivity of the light reflectors (iridophores) of the squid Alloteuthis subulata. The spectral changes that can be seen in living squid, can also be brought about by superfusing whole skin preparations with acetylcholine (ACh) (20 μmol l-1) and muscarine (30 μmol l-1) but not nicotine (up to 50 mmol l-1), suggesting that cholinergic muscarinic receptors are involved. Changing the osmolarity of the external solution had no effect on spectral reflectivity. To study the iridophores at the cellular level,iridophores were isolated enzymatically. Lucifer Yellow filled the iridophores uniformly, showing cellular individuality. Isolated iridophore cells were loaded with Fura-2 AM and cytoplasmic Ca2+ was recorded ratiometrically. Intracellular Ca2+ (resting concentration at 66.16 nmol l-1) increased transiently after addition of ACh (50 μmol l-1), muscarine (25 μmol l-1), but not nicotine (up to 5 mmol l-1). Ca2+ also increased when superfused with potassium chloride (10 mmol l-1) and caffeine (2.5 mmol l-1). Hypo- and hyperosmotic solutions had no effects on the cytoplasmic Ca2+. By presenting direct evidence that iridophores are polarised cellular structures containing Ca2+ stores and that they are activated via cholinergic muscarinic receptors, we demonstrate that Ca2+ is involved in the reflectivity changes of the iridophores of A. subulata. Specimens were prepared for transmission electron microscopy. It was found that the orientations of the plates with respect to the skin surface are in good agreement with the expected orientations based on the prediction that the iridophores act as multilayer reflectors.

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Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum

Cited by 1,757 publications

References 46 publications

REEP5 (Receptor Accessory Protein 5) Acts as a Sarcoplasmic Reticulum Membrane Sculptor to Modulate Cardiac Function

REEP5 (Receptor Accessory Protein 5) Acts as a Sarcoplasmic Reticulum Membrane Sculptor to Modulate Cardiac Function

Down-regulation of the cardiac sarcoplasmic reticulum ryanodine channel in severely food-restricted rats

The role of muscarinic receptors and intracellular Ca2+ in the spectral reflectivity changes of squid iridophores

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