Expression and Distribution of InsP3 Receptor Subtypes in Proliferating Vascular Smooth Muscle Cells

Tasker, Paul N.; Taylor, Colin W.; Nixon, Graeme F.

doi:10.1006/bbrc.2000.3036

Cited by 36 publications

(40 citation statements)

References 28 publications

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“…The distribution of IP3Rs is dependent on isoform and cell type as recently shown in, for example, pancreatic and salivary gland cells Zhang et al, 1999), oocytes (Fissore et al, 1999), aortic smooth muscle cells (Tasker et al, 2000) and aortic endothelial, adrenal glomerulosa and COS-7 cells (Laflamme et al, 2002). Differences in properties and distribution of IP3R isoforms can therefore determine the cellspecific pattern of the Ca 2+ signals (Hirata et al, 1999).…”

mentioning

confidence: 91%

Microtubule-dependent redistribution of the type-1 inositol 1,4,5-trisphosphate receptor in A7r5 smooth muscle cells

Vermassen

Acker

Annaert

et al. 2003

Journal of Cell Science

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IntroductionCellular activation by many agonists results in the stimulation of phospholipase C (PLC) and the subsequent hydrolysis of phosphatidylinositol 4,5-bisphosphate to inositol 1,4,5-trisphosphate (IP 3) and diacylglycerol (DAG) (Berridge, 1993). Each of these two molecules exerts a specific effect in the cell. The increased DAG concentration leads to the activation of protein kinase C (PKC) while IP3 binds to the IP3 receptor (IP3R), an intracellular Ca 2+ -release channel located in the endoplasmic reticulum (ER), thereby inducing Ca 2+ release from internal stores. A prolonged stimulation of cells with agonists, however, results in downregulation of the IP 3Rs and this appears to be a cell-and agonist-specific process (Sipma et al., 1998;Wojcikiewicz, 1995). This downregulation results from an accelerated IP3R degradation (Wojcikiewicz et al., 1994) and is mediated by the ubiquitin-proteasome pathway (Oberdorf et al., 1999). Ca 2+ signals evoked by agonist stimulation have complex temporal and spatial characteristics, and the underlying mechanisms are not yet fully understood (Berridge et al., 1998). The differential regulation of the IP3R isoforms by various modulators of IP 3-induced Ca 2+ release, such as IP3, cytosolic Ca 2+ , ATP, calmodulin and phosphorylation by several kinases,

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confidence: 91%

Microtubule-dependent redistribution of the type-1 inositol 1,4,5-trisphosphate receptor in A7r5 smooth muscle cells

Vermassen

Acker

Annaert

et al. 2003

Journal of Cell Science

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“…In addition, different IP 3 R subtypes could function redundantly in regulating vascular contractility and blood pressure, since it has been shown that all 3 subtypes are expressed in VSMCs (20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

IP3 receptors regulate vascular smooth muscle contractility and hypertension

et al. 2016

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“…cerebral artery smooth muscle cells; calcium wave; short hairpin RNA INOSITOL 1,4,5-trisphosphate (IP 3 ) receptors (IP 3 Rs) are expressed in many cell types and regulate several physiological functions, including development, muscle contraction, cell proliferation, and differentiation (1,45,47,56 Rs (7,43,54). IP 3 also activates cation channels in vascular smooth muscle cells through mechanisms that do not require the stimulation of sarcoplasmic reticulum (SR) Ca 2ϩ release (27, 54).…”

mentioning

confidence: 99%

“…INOSITOL 1,4,5-trisphosphate (IP 3 ) receptors (IP 3 Rs) are expressed in many cell types and regulate several physiological functions, including development, muscle contraction, cell proliferation, and differentiation (1,45,47,56). In vascular smooth muscle cells, IP 3 Rs modulate vasoconstriction and proliferation by altering spatial and temporal properties of local and global Ca 2ϩ signals (51,53).…”

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confidence: 99%

Type 1 inositol 1,4,5-trisphosphate receptors mediate UTP-induced cation currents, Ca²⁺ signals, and vasoconstriction in cerebral arteries

Zhao

Adebiyi²,

Blaskova

et al. 2008

American Journal of Physiology-Cell Physiology

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,4,5-trisphosphate receptors (IP3Rs) regulate diverse physiological functions, including contraction and proliferation. There are three IP3R isoforms, but their functional significance in arterial smooth muscle cells is unclear. Here, we investigated relative expression and physiological functions of IP3R isoforms in cerebral artery smooth muscle cells. We show that 2-aminoethoxydiphenyl borate and xestospongin C, membrane-permeant IP3R blockers, reduced Ca 2ϩ wave activation and global intracellular Ca 2ϩ ([Ca 2ϩ ]i) elevation stimulated by UTP, a phospholipase C-coupled purinergic receptor agonist. Quantitative PCR, Western blotting, and immunofluorescence indicated that all three IP3R isoforms were expressed in acutely isolated cerebral artery smooth muscle cells, with IP3R1 being the most abundant isoform at 82% of total IP3R message. IP3R1 knockdown with short hairpin RNA (shRNA) did not alter baseline Ca 2ϩ wave frequency and global [Ca 2ϩ ]i but abolished UTP-induced Ca 2ϩ wave activation and reduced the UTP-induced global [Ca 2ϩ ]i elevation by ϳ61%. Antibodies targeting IP3R1 and IP3R1 knockdown reduced UTP-induced nonselective cation current (Icat) activation. IP3R1 knockdown also reduced UTP-induced vasoconstriction in pressurized arteries with both intact and depleted sarcoplasmic reticulum (SR) Ca 2ϩ by ϳ45%. These data indicate that IP 3R1 is the predominant IP3R isoform expressed in rat cerebral artery smooth muscle cells. IP 3R1 stimulation contributes to UTP-induced I cat activation, Ca 2ϩ wave generation, global [Ca 2ϩ ]i elevation, and vasoconstriction. In addition, IP 3R1 activation constricts cerebral arteries in the absence of SR Ca 2ϩ release by stimulating plasma membrane Icat.cerebral artery smooth muscle cells; calcium wave; short hairpin RNA INOSITOL 1,4,5-trisphosphate (IP 3 ) receptors (IP 3 Rs) are expressed in many cell types and regulate several physiological functions, including development, muscle contraction, cell proliferation, and differentiation (1,45,47,56 Rs (7,43,54). IP 3 also activates cation channels in vascular smooth muscle cells through mechanisms that do not require the stimulation of sarcoplasmic reticulum (SR) Ca 2ϩ release (27, 54). In cerebral artery smooth muscle cells, IP 3 R activation stimulates TRPC3 channels, leading to Na ϩ influx, membrane depolarization, voltage-dependent Ca 2ϩ channel activation, and vasoconstriction (54). Thus IP 3 Rs regulate ion channel activity, Ca 2ϩ signals, and physiological functions in the vasculature. However, despite the functional importance of IP 3 Rs in arterial smooth muscle cells, specific IP 3 R isoforms that are expressed in this cell type and their functional significance are poorly understood.Three IP 3 R isoforms, designated IP 3 R1, IP 3 R2, and IP 3 R3, are encoded by distinct genes (6, 37). IP 3 R isoform expression varies widely between different cell types. Cerebellar Purkinje neurons express predominantly IP 3 R1, pancreatic ␤-cells primarily express IP 3 R3, and cardiac myocytes express IP 3 R2 (14, 48...

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Expression and Distribution of InsP3 Receptor Subtypes in Proliferating Vascular Smooth Muscle Cells

Cited by 36 publications

References 28 publications

Microtubule-dependent redistribution of the type-1 inositol 1,4,5-trisphosphate receptor in A7r5 smooth muscle cells

Microtubule-dependent redistribution of the type-1 inositol 1,4,5-trisphosphate receptor in A7r5 smooth muscle cells

IP3 receptors regulate vascular smooth muscle contractility and hypertension

Type 1 inositol 1,4,5-trisphosphate receptors mediate UTP-induced cation currents, Ca²⁺ signals, and vasoconstriction in cerebral arteries

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Expression and Distribution of InsP3 Receptor Subtypes in Proliferating Vascular Smooth Muscle Cells

Cited by 36 publications

References 28 publications

Microtubule-dependent redistribution of the type-1 inositol 1,4,5-trisphosphate receptor in A7r5 smooth muscle cells

Microtubule-dependent redistribution of the type-1 inositol 1,4,5-trisphosphate receptor in A7r5 smooth muscle cells

IP3 receptors regulate vascular smooth muscle contractility and hypertension

Type 1 inositol 1,4,5-trisphosphate receptors mediate UTP-induced cation currents, Ca2+ signals, and vasoconstriction in cerebral arteries

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Type 1 inositol 1,4,5-trisphosphate receptors mediate UTP-induced cation currents, Ca²⁺ signals, and vasoconstriction in cerebral arteries