Cellular Mechanisms Regulating [Ca2+]i Smooth Muscle

Breemen, Cornelis van; Saida, Kooichi

doi:10.1146/annurev.ph.51.030189.001531

Cited by 372 publications

(122 citation statements)

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“…Indeed, according to this model, the Ca 2ϩ influx is thought to be regulated by the Ca 2ϩ content of intracellular pools. The importance of SERCAs in this capacitative entry was suggested, since this theory comes from the observation that inhibitors of SERCA, such as thapsigargin, cause depletion of intracellular Ca 2ϩ pools (without IP 3 formation and as a result, mimic the ability of surface membrane, IP 3 agonists, to activate Ca 2ϩ entry) (50). Now, we might suggest the physiological role of SERCAs in the Ca 2ϩ signaling cascade by their function of refilling Ca 2ϩ stores following store depletion and Ca 2ϩ influx, as the further essential step in Ca 2ϩ movements associated with PDGF-induced SMC proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…2 and 3). Ca 2ϩ channels in the plasma membrane allow Ca 2ϩ influx following a stimulation due to membrane depolarization (voltage-operated channels) (3,4) or binding of a ligand to its receptor (receptoroperated channels) (5). Intracellular Ca 2ϩ pools are also strongly implicated in the increase in cytosolic Ca 2ϩ concentration by liberating their Ca 2ϩ content into the cytosol through intracellular Ca 2ϩ channels: the inositol 1,4,5-trisphosphate (IP 3 ) 1 receptor (6) and the ryanodine receptor (7).…”

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confidence: 99%

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Smooth Muscle Cell Cycle and Proliferation

Magnier-Gaubil

Herbert

Quarck

et al. 1996

Journal of Biological Chemistry

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The role of Ca 2؉ influx in the regulation of the sarcoendoplasmic reticulum Ca 2؉ ATPases (SERCA) associated with intracellular Ca 2؉ pools was investigated during smooth muscle cell (SMC) proliferation induced by platelet-derived growth factor (PDGF). We first defined that the previously described up-regulation of the SERCA2a isoform found in vascular SMC after a 24-h stimulation with PDGF (Magnier, C., Papp, B., Corvazier, E., Bredoux, R., Wuytack, F., Eggermont, F., Maclouf, J., and Enouf, J. (

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Smooth Muscle Cell Cycle and Proliferation

Magnier-Gaubil

Herbert

Quarck

et al. 1996

Journal of Biological Chemistry

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“…Since the intracellular concentration of Ca 2+ ([Ca2+]i) is a major determinant of contractile force, much effort has been devoted to elucidating mechanisms which regulate [CaZ+]~ in smooth muscle [1,2]. It is now clear that multiple and complex signaling pathways participate in these mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Receptor‐activated increases in intracellular calcium and protein tyrosine phosphorylation in vascular smooth muscle cells

Semenchuk

Salvo

1995

FEBS Letters

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To more directly test the hypothesis that a functional link exists between receptor-activated increases in [Ca2÷], and protein tyrosine phosphorylation in smooth muscle cells, we studied interrelationships among receptor-activation of cultured VSMC, increases in [Ca-~+]~, and enhanced protein tyrosine phosphorylation. We report that increases in [Ca2+]~ evoked by stimulation of ~-adrenergic receptors with phenylephrine or serotoninergic receptors with serotonin are associated with enhanced protein tyrosine phosphorylation of several substrates. One of the substrates is rasGAP, the GTPase Activating Protein for the small G-protein called ras. We also report that genistein, a potent inhibitor of tyrosine kinases [10] reversibly inhibits receptor-activated increases in [Ca2+]~ and enhanced tyrosine phosphorylation of rasGAP. These observations suggest that a signaling pathway for increasing [Ca2+]i in VSMC probably involves receptor activation, enhanced tyrosine phosphorylation of rasGAP and the participation of a small G-protein such as ras.

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“…VSMC contraction is triggered by a rise of cytosolic calcium ion concentration ([Ca 2ϩ ]) due to either transmembrane Ca 2ϩ influx or Ca 2ϩ release from the sarcoplasmic reticulum (SR). Extracellular Ca 2ϩ entry normally occurs through L-type voltagedependent Ca 2ϩ channels, although there are numerous ligandgated membrane channels that are also Ca 2ϩ permeable (1). Ca 2ϩ release from the SR is mediated by inositol trisphosphate (InsP 3 ) and ryanodine receptors.…”

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confidence: 99%

Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction

Valle‐Rodríguez

Calderón

Ruiz

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Voltage-gated Ca 2؉ channels in arterial myocytes can mediate Ca 2؉ release from the sarcoplasmic reticulum and, thus, induce contraction without the need of extracellular Ca 2؉ influx. This metabotropic action of Ca 2؉ channels (denoted as calcium-channelinduced calcium release or CCICR) involves activation of G proteins and the phospholipase C-inositol 1,4,5-trisphosphate pathway. Here, we show a form of vascular tone regulation by extracellular ATP that depends on the modulation of CCICR. In isolated arterial myocytes, ATP produced facilitation of Ca 2؉ -channel activation and, subsequently, a strong potentiation of CCICR. The facilitation of L-type channel still occurred after full blockade of purinergic receptors and inhibition of G proteins with GDP␤S, thus suggesting that ATP directly interacts with Ca 2؉ channels. The effects of ATP appear to be highly selective, because they were not mimicked by other nucleotides (ADP or UTP) or vasoactive agents, such as norepinephrine, acetylcholine, or endothelin-1. We have also shown that CCICR can trigger arterial cerebral vasoconstriction in the absence of extracellular calcium and that this phenomenon is greatly facilitated by extracellular ATP. Although, at low concentrations, ATP does not induce arterial contraction per se, this agent markedly potentiates contractility of partially depolarized or primed arteries. Hence, the metabotropic action of L-type Ca 2؉ channels could have a high impact on vascular pathophysiology, because, even in the absence of Ca 2؉ channel opening, it might mediate elevations of cytosolic Ca 2؉ and contraction in partially depolarized vascular smooth muscle cells exposed to small concentrations of agonists.L-type Ca 2ϩ channel ͉ vascular contractility ͉ excitation-contraction coupling C ontraction of vascular smooth muscle cells (VSMCs) determines vessel diameter and, thus, regulates blood flow and pressure. VSMC contraction is triggered by a rise of cytosolic calcium ion concentration ([Ca 2ϩ ]) due to either transmembrane Ca 2ϩ influx or Ca 2ϩ release from the sarcoplasmic reticulum (SR). Extracellular Ca 2ϩ entry normally occurs through L-type voltagedependent Ca 2ϩ channels, although there are numerous ligandgated membrane channels that are also Ca 2ϩ permeable (1). Ca 2ϩ release from the SR is mediated by inositol trisphosphate (InsP 3 ) and ryanodine receptors. Vasoactive agents acting on the different vascular territories induce VSMC contraction by binding to membrane receptors and the subsequent activation of one or more of the Ca 2ϩ -entry and͞or Ca 2ϩ -release channels (2-5).We have described a previously unnoticed metabotropic effect of vascular L-type Ca 2ϩ channels, denoted as calcium-channelinduced Ca 2ϩ release (CCICR), which requires Ca 2ϩ channel activation but is independent of extracellular Ca 2ϩ influx (6). This new Ca 2ϩ -release mechanism depends on the conformational change of L-type Ca 2ϩ channels and the downstream activation of the G protein͞phospholipase C (PLC) cascade, leading to synthesis of InsP 3 and C...

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Cellular Mechanisms Regulating [Ca2+]i Smooth Muscle

Cited by 372 publications

References 58 publications

Smooth Muscle Cell Cycle and Proliferation

Smooth Muscle Cell Cycle and Proliferation

Receptor‐activated increases in intracellular calcium and protein tyrosine phosphorylation in vascular smooth muscle cells

Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction

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Cellular Mechanisms Regulating [Ca2+]i Smooth Muscle

Cited by 372 publications

References 58 publications

Smooth Muscle Cell Cycle and Proliferation

Smooth Muscle Cell Cycle and Proliferation

Receptor‐activated increases in intracellular calcium and protein tyrosine phosphorylation in vascular smooth muscle cells

Metabotropic Ca 2+ channel-induced Ca 2+ release and ATP-dependent facilitation of arterial myocyte contraction

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Product

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Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction