Requirement of Ryanodine Receptor Subtypes 1 and 2 for Ca2+-induced Ca2+ Release in Vascular Myocytes

Coussin, Frédéric; Macrez, Nathalie; Morel, Jean-Luc; Mironneau, Jean

doi:10.1074/jbc.275.13.9596

Cited by 116 publications

(149 citation statements)

References 45 publications

Supporting

Mentioning

131

Contrasting

Order By: Relevance

“…The role of RyR2 in Ca 2ϩ spark signaling has been extensively studied in the heart, but we know the least about the role of RyR3 in the generation of Ca 2ϩ sparks in SMCs. RyR3 gene knockout or knockdown does not alter local Ca 2ϩ signaling in bladder and portal vein SMCs (8,17); yet, it has been reported that the frequency of STOCs is augmented in RyR3 Ϫ/Ϫ cerebral artery myocytes (27). This result has been interpreted as evidence for the inhibitory role of RyR3 in the development of Ca 2ϩ sparks, since STOCs are generally thought to be activated by Ca 2ϩ sparks.…”

Section: Discussionmentioning

confidence: 72%

“…As a consequence, RyR1 full expression is required for the CaN-based regulation of local Ca 2ϩ signaling in ASMCs. In support, RyR1 is also required for the Ca 2ϩ spark formation in skeletal muscle cells (35), depolarization-induced Ca 2ϩ spark in cultured portal vein (8), and embryonic bladder SMCs (11). RyR1 Ϫ/ϩ ASMCs have a lower level of local Ca 2ϩ signaling, further indicating the specific importance of RyR1 in this cell type.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells

Savoia

Liu

Zheng

et al. 2014

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells

Savoia

Liu

Zheng

et al. 2014

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

show abstract

“…Although activation of the SR Ca 2+ release by Ca 2+ entering the cell via VGCCs has been demonstrated in voltage-clamp experiments performed on different types of visceral and vascular SMCs (Kamishima and McCarron, 1997;Kohda et al, 1997;Bolton and Gordienko, 1998;Shmigol et al, 1998;Coussin et al, 2000), there is a number of studies (e.g. Bradley et al, 2002;2004) (Bradley et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…In this study we have demonstrated that in RVSMCs 2-APB exerts no effect on the Ca 2+ entry mechanisms induced by P2X receptor activation and the SR calcium load ( Figure 5). Because the effect of 2-APB on ab-meATP-induced [Ca 2+ ]i transient was significantly attenuated in the presence of nicardipine, we concluded that in RVSMCs IP3R-mediated Ca 2+ release following P2X receptor stimulation is activated mainly by Ca 2+ entering the cell via VGCCs.Although activation of the SR Ca 2+ release by Ca 2+ entering the cell via VGCCs has been demonstrated in voltage-clamp experiments performed on different types of visceral and vascular SMCs (Kamishima and McCarron, 1997;Kohda et al, 1997;Bolton and Gordienko, 1998;Shmigol et al, 1998;Coussin et al, 2000), there is a number of studies (e.g. Bradley et al, 2002;2004) (Bradley et al, 2004).…”

mentioning

confidence: 99%

Ca²⁺ entry following P2X receptor activation induces IP₃ receptor‐mediated Ca²⁺ release in myocytes from small renal arteries

Povstyan

Harhun

Gordienko

2011

British J Pharmacology

View full text Add to dashboard Cite

BACKGROUND AND PURPOSEP2X receptors mediate sympathetic control and autoregulation of the renal circulation triggering contraction of renal vascular smooth muscle cells (RVSMCs) via an elevation of intracellular Ca 2+ concentration ([Ca 2+ ]i). Although it is well-appreciated that the myocyte Ca 2+ signalling system is composed of microdomains, little is known about the structure of the [Ca 2+ ]i responses induced by P2X receptor stimulation in vascular myocytes. EXPERIMENTAL APPROACHESUsing confocal microscopy, perforated-patch electrical recordings, immuno-/organelle-specific staining, flash photolysis and RT-PCR analysis we explored, at the subcellular level, the Ca 2+ signalling system engaged in RVSMCs on stimulation of P2X receptors with the selective agonist ab-methylene ATP (ab-meATP). KEY RESULTSRT-PCR analysis of single RVSMCs showed the presence of genes encoding inositol 1,4,5-trisphosphate receptor type 1(IP3R1) and ryanodine receptor type 2 (RyR2). The amplitude of the [Ca 2+ ]i transients depended on ab-meATP concentration. Depolarization induced by 10 mmol·L -1 ab-meATP triggered an abrupt Ca 2+ release from sub-plasmalemmal ('junctional') sarcoplasmic reticulum enriched with IP3Rs but poor in RyRs. Depletion of calcium stores, block of voltage-gated Ca 2+ channels (VGCCs) or IP3Rs suppressed the sub-plasmalemmal [Ca 2+ ]i upstroke significantly more than block of RyRs. The effect of calcium store depletion or IP3R inhibition on the sub-plasmalemmal [Ca 2+ ]i upstroke was attenuated following block of VGCCs. CONCLUSIONS AND IMPLICATIONSDepolarization of RVSMCs following P2X receptor activation induces IP3R-mediated Ca 2+ release from sub-plasmalemmal ('junctional') sarcoplasmic reticulum, which is activated mainly by Ca 2+ influx through VGCCs. This mechanism provides convergence of signalling pathways engaged in electromechanical and pharmacomechanical coupling in renal vascular myocytes. Abbreviations2-APB, 2-aminoethoxydiphenyl borate; ab-meATP, ab-methylene ATP; CICR, Ca 2+ -induced Ca 2+ release; CPA, cyclopiazonic acid; IP3, inositol 1,4,5-trisphosphate; IP3R, inositol 1,4,5-trisphosphate receptor; jSR, sub-plasmalemmal ('junctional') sarcoplasmic reticulum; MRS2578, N,N' NF279, 8,] bis(1,3,5-naphthalene-trisulphonic acid); PLC, phospholipase C; RBF, renal blood flow; RSNA, renal sympathetic nerve activity; RT-PCR, reverse transcription polymerase chain reaction; RVSMC, renal vascular smooth muscle cells; RyR, ryanodine receptor; SERCA, sarco-/endoplasmic reticulum Ca 2+ -ATPase; SPCU, sub-plasmalemmal [Ca 2+ ]i upstroke; SR, sarcoplasmic reticulum; U-73122, 1-[6-([(17b)-3-methoxyestra-1,3,5(10) IntroductionRenal blood flow (RBF) accounts for 20-25% of cardiac output at rest (Malpas and Leonard, 2000;Cupples and Braam, 2007). The mechanisms controlling contraction/relaxation of renal vascular smooth muscle cells (RVSMCs), which regulate the diameter of renal resistance arteries and hence RBF and glomerular filtration rate, play a fundamental role in the control of systemic blood pr...

show abstract

“…The control No RT reactions were PCR amplified to ensure that DNA did not contaminate RNA. One microliter of cDNA was then amplified using 1 µM of each primer, 1X PCR buffer minus Mg, 5 mM MgCl 2 , 1 mM deoxyribonucleotide triphosphates, and 2 units of Platinum ® Taq DNA Polymerase in a final volume of (12) and Coussin et al (13). Preliminary experiments were conducted with each gene to determine the number of PCR cycles that represented the linear range of amplification.…”

mentioning

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

View full text Add to dashboard Cite

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

show abstract

Requirement of Ryanodine Receptor Subtypes 1 and 2 for Ca2+-induced Ca2+ Release in Vascular Myocytes

Abstract: While the roles of subtypes 1 and 2 of the ryanodine receptors (RYRs) have been studied in cellular systems expressing specifically one or the other of these subtypes (i.e. skeletal and cardiac muscle), the function of these receptors has not been evaluated in smooth muscles.

Cited by 116 publications

References 45 publications

Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells

Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells

Ca²⁺ entry following P2X receptor activation induces IP₃ receptor‐mediated Ca²⁺ release in myocytes from small renal arteries

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

Contact Info

Product

Resources

About

Requirement of Ryanodine Receptor Subtypes 1 and 2 for Ca2+-induced Ca2+ Release in Vascular Myocytes

Abstract: While the roles of subtypes 1 and 2 of the ryanodine receptors (RYRs) have been studied in cellular systems expressing specifically one or the other of these subtypes (i.e. skeletal and cardiac muscle), the function of these receptors has not been evaluated in smooth muscles.

Cited by 116 publications

References 45 publications

Calcineurin upregulates local Ca2+signaling through ryanodine receptor-1 in airway smooth muscle cells

Calcineurin upregulates local Ca2+signaling through ryanodine receptor-1 in airway smooth muscle cells

Ca2+ entry following P2X receptor activation induces IP3 receptor‐mediated Ca2+ release in myocytes from small renal arteries

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

Contact Info

Product

Resources

About

Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells

Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells

Ca²⁺ entry following P2X receptor activation induces IP₃ receptor‐mediated Ca²⁺ release in myocytes from small renal arteries