The aminosteroid U-73122 inhibits muscarinic receptor sequestration and phosphoinositide hydrolysis in SK-N-SH neuroblastoma cells. A role for Gp in receptor compartmentation.

Thompson, A.; Mostafapour, Sam P.; Denlinger, Loren C.; Bleasdale, John E.; Fisher, Stephen K.

doi:10.1016/s0021-9258(18)54362-3

Cited by 407 publications

(40 citation statements)

References 11 publications

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“…U73122 did not alter basal [Ca 2 + ] i . The inactive U73122 analogue U73313 23 did not alter ATP-induced [Ca 2 + ] i increase, suggesting that U73122 effectively inhibited phospholipase C activity. Figure 3B further shows that addition of 50 •M triethyltin subsequently to U73122 and ATP pretreatment induced a [Ca 2 + ] i increase indistinguishable from the control triethyltin response shown in Figure 2C (n=4, P>0.05).…”

Section: Resultsmentioning

confidence: 94%

“…U73122 is an effective inhibitor of phospholipase C in many cell types. 23 Figure 3A shows that in Ca 2 + -free medium, the inositol 1,4,5-trisphosphate-dependent Ca 2 + mobilizer ATP induced a [Ca 2 + ] i increase with a net maximum of 121 ‹ 5 nM (n=4). This ATP response was abolished by pretreatment with 2 •M U73122 for 6 min (Figure 3B; n=4).…”

Section: Resultsmentioning

confidence: 99%

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Effect of triethyltin on Ca2+ movement in Madin–Darby canine kidney cells

Jiann

et al. 2002

Hum Exp Toxicol

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The effects of the environmental toxicant, triethyltin, on Ca2 + mobilization in Madin–Darby canine kidney (MDCK) cells have been examined. Triethyltin induced an increase in cytosolic free Ca2 + levels ([Ca2 +]i) at concentrations larger than 2 mM in a concentrationdependent manner. Within 5 min, the [Ca2 +]i signal was composed of a gradual rise and a sustained phase. The [Ca2 +]i signal was partly reduced by removing extracellular Ca2 +. In Ca2 +-free medium, pretreatment with thapsigargin (1 mM), an endoplasmic reticulum Ca2 + pump inhibitor, reduced 50 mM triethyltin-induced [Ca2 +]i increase by 80%. Conversely, pretreatment with triethyltin abolished thapsigargin-induced Ca2 + release. Pretreatment with U73122 (2 mM) to inhibit phospholipase C-coupled inositol 1,4,5-trisphosphate formations failed to alter 50 mM triethyltin-induced Ca2 + release. Incubation with triethyltin at a concentration (1 mM) that did not increase basal [Ca2 +]i for 3 min did not alter ATP (10 mM)and bradykinin (1 mM)-induced [Ca2 +]i increases. Collectively, this study shows that triethyltin altered Ca2 + movement in renal tubular cells by releasing Ca2 + from multiple stores in an inositol 1,4,5-trisphosphate-independent manner, and by inducing Ca2 + influx.

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Section: Resultsmentioning

confidence: 94%

Section: Resultsmentioning

confidence: 99%

Effect of triethyltin on Ca2+ movement in Madin–Darby canine kidney cells

Jiann

et al. 2002

Hum Exp Toxicol

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“…This suggests the presence of an inositol 1,4,5 -trisphosphate-coupled Ca 2+ -mobilizing machinery in HA22 /VGH cells. Figure 3B shows that addition of 2 M U73122, a phospholipase C inhibitor, 25 for 230 s to inhibit phospholipase C did not affect basal [Ca 2+ ] i , but abolished 5 M histamine -induced [Ca 2+ ] i increases ( n =4 ). Conversely, U73343 (10 M), a U73122 analogue that does not inhibit phospholipase C, had no effect ( n =4; not shown ).…”

Section: Resultsmentioning

confidence: 98%

Effects of the antianginal drug fendiline on Ca2+ movement in hepatoma cells

Cheng¹,

Wang²,

Lo³

et al. 2001

Hum Exp Toxicol

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This study investigated the effect of the anti-anginal drug, fendiline, on intracellular free Ca2+ levels ([Ca2+]i)inHA/ 22 human hepatoma cells by using fura-2 as a fluorescent Ca2+ dye. Fendiline (1-100 μM) increased [Ca2+]i with an EC50 of 25 μM. Removal of extracellular Ca2+ reduced the [Ca2+]i signals by 51-5%. Fendiline (10 μM)-induced Ca2+release was abolished by pretreatment with 1 μM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor). Inhibition of phospholipase C with 2 μM 1-(6-((17β 3 methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H pyrrole-2,5-dione (U73122) did not alter 10 μM fendilineinducedCa2+ release.Severalothercalmodulinantagonists, such as phenoxybenzamine (100-200 μM), trifluoperazine (5-50 μM),andfluphenazine N-chloroethane(2-100 μM), hadno effect on[Ca2+]i. Together, it wasfound that fendiline increased [Ca2+]i in human hepatoma cells by discharging Ca2+ from the endoplasmic reticulum in an inositol 1,4,5 trisphosphate-independent manner and by inducing Ca2+entry. This effect of fendiline does not appear to be via antagonism of calmodulin.

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“…12,13 Because m-3M3FBS was able to release Ca 2þ from the endoplasmic reticulum, the role of PLC in this release was examined. U73122, a PLC inhibitor, 25 was applied to see whether this enzyme was required for m-3M3FBS-induced Ca 2þ release. Figure 5A shows that ATP (10 mM) induced a [Ca 2þ ] i rise of 69 nM.…”

Section: Resultsmentioning

confidence: 99%

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

et al. 2009

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The effect of 2,4,6-trimethyl-N-(meta-3-trifluoromethyl-phenyl)-benzenesulfonamide (m-3M3FBS), a presumed phospholipase C (PLC) activator, on cytosolic free Ca2+ concentrations ([Ca 2+]i) in Madin-Darby canine kidney (MDCK) cells is unclear. This study explored whether m-3M3FBS changed basal [Ca2+]i levels in suspended MDCK cells using fura-2 as a Ca2+-sensitive fluorescent dye. M-3M3FBS at concentrations between 0.1 and 20 μM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was decreased 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, 20-μM m-3M3FBS pretreatment abolished the [Ca2+]i rise induced by the endoplasmic reticulum Ca2+ pump inhibitors thapsigargin (TG) and cyclopiazonic acid (CPA). Conversely, pretreatment with TG or CPA partly reduced m-3M3FBS-induced [Ca2+]i rise. The inhibition of PLC with U73122 did not alter m-3M3FBS-induced [Ca2+]i rise. Collectively, in MDCK cells, m-3M3FBS induced [Ca2+]i rises by causing PLC-independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx via store-operated Ca2+ channels and other unidentified Ca2+ channels.

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The aminosteroid U-73122 inhibits muscarinic receptor sequestration and phosphoinositide hydrolysis in SK-N-SH neuroblastoma cells. A role for Gp in receptor compartmentation.

Cited by 407 publications

References 11 publications

Effect of triethyltin on Ca2+ movement in Madin–Darby canine kidney cells

Effect of triethyltin on Ca2+ movement in Madin–Darby canine kidney cells

Effects of the antianginal drug fendiline on Ca2+ movement in hepatoma cells

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

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