Effect of m-3M3FBS on Ca2+ movement in Madin-Darby canine renal tubular cells

Fang, Yi-Chien; Kuo, Daih‐Huang; Shieh, Pochuen; Chen, Fu‐An; Kuo, Chun-Chi; Jan, Chung‐Ren

doi:10.1177/0960327109106972

Cited by 4 publications

(1 citation statement)

References 42 publications

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“…m -3M3-FBS acts on all isoforms of PLC and treatment has been shown to increase cellular IP 3 and elevate cytosolic Ca 2+ consistent with stimulation of PLC activity 29; 30 as illustrated in panel A . Transfection conditions were used such that comparable levels of WT-and P7L VLP were obtained from untreated cells ( panel B top, lanes 1 and 5 ).…”

Section: Resultsmentioning

confidence: 72%

ESCRT Machinery Potentiates HIV-1 Utilization of the PI(4,5)P2-PLC-IP3R-Ca2+ Signaling Cascade

Ehrlich

Medina

Carter

2011

Journal of Molecular Biology

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HIV-1 release efficiency is directed by late (L) domain motifs in the viral structural precursor polyprotein, Gag, which serve as links to the ESCRT (endocytic sorting complex required for transport) machinery. Linkage is normally through binding of Tsg101, an ESCRT-1 component, to the P7TAP motif in the p6 region of Gag. In its absence, budding is directed by binding of Alix, an ESCRT adaptor protein, to the LY36PXnL motif in Gag. We recently showed that budding requires activation of the inositol 1,4,5-triphosphate receptor (IP3R), a protein that “gates” Ca2+ release from intracellular stores, triggers Ca2+ cell influx and thereby functions as a major regulator of Ca2+ signaling. In the present study, we determined whether the L domain links Gag to Ca2+ signaling machinery. Depletion of IP3R and inactivation of phospholipase C (PLC) inhibited budding whether or not Tsg101 was bound to Gag. PLC hydrolysis of PI(4,5)P2 generates IP3, the ligand that activates IP3R. However, with Tsg101 bound, Gag release was independent of Gq-mediated activation of PLC and budding was readily enhanced by pharmacological stimulation of PLC. Moreover, IP3R was redistributed to the cell periphery and cytosolic Ca2+ was elevated, events indicative of induction of Ca2+ signaling. The results suggest that L domain function, ESCRT machinery, and Ca2+signaling are linked events in Gag release.

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Section: Resultsmentioning

confidence: 72%

ESCRT Machinery Potentiates HIV-1 Utilization of the PI(4,5)P2-PLC-IP3R-Ca2+ Signaling Cascade

Ehrlich

Medina

Carter

2011

Journal of Molecular Biology

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Effect ofm-3m3FBS on Ca²⁺handling and viability in OC2 human oral cancer cells

Chi

Chou²,

Kuo³

et al. 2012

Acta Physiologica Hungarica

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The effect of 2,4,6-trimethyl-N-(meta-3-trifluoromethyl-phenyl)-benzenesulfonamide (m-3M3FBS), a presumed phospholipase C activator, on cytosolic free Ca2+ concentrations ([Ca2+]i) in OC2 human oral cancer cells is unclear. This study explored whether m-3M3FBS changed basal [Ca2+]i levels in suspended OC2 cells by using fura-2 as a Ca2+-sensitive fluorescent dye. M-3M3FBS at concentrations between 10-60 μM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced partly by removing extracellular Ca2+. M-3M3FBS-induced Ca2+ influx was inhibited by the store-operated Ca2+ channel blockers nifedipine, econazole and SK&F96365, and by the phospholipase A2 inhibitor aristolochic acid. In Ca2+-free medium, 30 μM m-3M3FBS pretreatment inhibited the [Ca2+]i rise induced by the endoplasmic reticulum Ca2+ pump inhibitors thapsigargin and 2,5-di-tert-butylhydroquinone (BHQ). Conversely, pretreatment with thapsigargin, BHQ or cyclopiazonic acid partly reduced m-3M3FBS-induced [Ca2+]i rise. Inhibition of inositol 1,4,5-trisphosphate formation with U73122 did not alter m-3M3FBS-induced [Ca2+]i rise. At concentrations between 5 and 100 μM m-3M3FBS killed cells in a concentration-dependent manner. The cytotoxic effect of m-3M3FBS was not reversed by prechelating cytosolic Ca2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA). Propidium iodide staining data suggest that m-3M3FBS (20 or 50 μM) induced apoptosis in a Ca2+-independent manner. Collectively, in OC2 cells, m-3M3FBS induced [Ca2+]i rise by causing inositol 1,4,5-trisphosphate-independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx via phospholipase A2-sensitive store-operated Ca2+ channels. M-3M3FBS also induced Ca2+-independent cell death and apoptosis.

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M-3M3FBS-Induced Ca^(2+) Movement and Apoptosis in HA59T Human Hepatoma Cells

Liu

Lin²,

Lu³

et al. 2013

Chin. J. Physiol.

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The effect of 2,4,6-trimethyl-N-(meta-3-trifluoromethyl-phenyl)-benzenesulfonamide (m-3M3FBS), a presumed phospholipase C activator, on cytosolic free Ca² ⁺ concentrations ([Ca² ⁺ ]i ) in HA59T human hepatoma cells is unclear. This study explored whether m-3M3FBS elevated basal [Ca² ⁺ ]i levels in suspended cells by using fura-2 as a Ca² ⁺ -sensitive fluorescent dye. M-3M3FBS at concentrations of 10- 50 μM increased [Ca² ⁺ ]i in a concentration-dependent fashion. The Ca² ⁺ signal was reduced partly by removing extracellular Ca² ⁺ . M-3M3FBS-induced Ca² ⁺ influx was inhibited by nifedipine, econazole, SK&F96365, aristolochic acid, and GF109203X. In Ca² ⁺ -free medium, 50 μM m-3M3FBS pretreatment inhibited the [Ca² ⁺ ]i rise induced by the endoplasmic reticulum Ca² ⁺ pump inhibitor thapsigargin. Conversely, pretreatment with thapsigargin partly reduced m-3M3FBS-induced [Ca² ⁺ ]i rise. Inhibition of inositol 1,4,5-trisphosphate formation with U73122 did not alter m-3M3FBS-induced [Ca² ⁺ ]i rise. At concentrations between 10 and 40 μM m-3M3FBS killed cells in a concentration-dependent manner. The cytotoxic effect of m-3M3FBS was not reversed by prechelating cytosolic Ca² ⁺ with 1,2-bis(2- aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA). Annexin V/propidium iodide staining data suggest that m-3M3FBS induced apoptosis in a concentration-dependent manner. M-3M3FBS also increased levels of reactive oxygen species. Together, in human hepatoma cells, m-3M3FBS induced a [Ca² ⁺ ]i rise by inducing phospholipase C-independent Ca² ⁺ release from the endoplasmic reticulum and Ca² ⁺ entry via protein kinase C-sensitive store-operated Ca² ⁺ channels. M-3M3FBS induced cell death that might involve apoptosis via mitochondrial pathways.

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Effect of m-3M3FBS on Ca2+ movement in Madin-Darby canine renal tubular cells

Cited by 4 publications

References 42 publications

ESCRT Machinery Potentiates HIV-1 Utilization of the PI(4,5)P2-PLC-IP3R-Ca2+ Signaling Cascade

ESCRT Machinery Potentiates HIV-1 Utilization of the PI(4,5)P2-PLC-IP3R-Ca2+ Signaling Cascade

Effect ofm-3m3FBS on Ca²⁺handling and viability in OC2 human oral cancer cells

M-3M3FBS-Induced Ca^(2+) Movement and Apoptosis in HA59T Human Hepatoma Cells

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Effect of m-3M3FBS on Ca2+ movement in Madin-Darby canine renal tubular cells

Cited by 4 publications

References 42 publications

ESCRT Machinery Potentiates HIV-1 Utilization of the PI(4,5)P2-PLC-IP3R-Ca2+ Signaling Cascade

ESCRT Machinery Potentiates HIV-1 Utilization of the PI(4,5)P2-PLC-IP3R-Ca2+ Signaling Cascade

Effect ofm-3m3FBS on Ca2+handling and viability in OC2 human oral cancer cells

M-3M3FBS-Induced Ca^(2+) Movement and Apoptosis in HA59T Human Hepatoma Cells

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Effect ofm-3m3FBS on Ca²⁺handling and viability in OC2 human oral cancer cells