Mechanism underlying histamine-induced intracellular Ca2+ movement in PC3 human prostate cancer cells
Department of Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, Republic of China. Pharmacological Research
(Impact Factor: 4.41).
01/2002; 44(6):547-52. DOI: 10.1006/phrs.2001.0891
The effect of histamine on intracellular free Ca2+ levels ([Ca2+]i) in PC3 human prostate cancer cells and the underlying mechanism were evaluated using fura-2 as a Ca2+ dye. Histamine at concentrations between 0.1 and 50 microM increased [Ca2+]i in a concentration-dependent manner with an EC50 value of 1 microM. The [Ca2+]i response comprised an initial rise and a slow decay, which returned to baseline within 3 min. Extracellular Ca2+ removal inhibited 50% of the [Ca2+]i signal. In the absence of extracellular Ca2+, after cells were treated with 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), 10 microM histamine did not increase [Ca2+]i. After pretreatment with 10 microM histamine in a Ca2+-free medium for several minutes, addition of 3 mM Ca2+ induced [Ca2+]i increases. Histamine (10 microM)-induced intracellular Ca2+ release was abolished by inhibiting phospholipase C with 2 microM 1-(6-((17 beta-3- methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122), and by 10 microM pyrilamine but was not altered by 50 microM cimetidine. Collectively, the present study shows that histamine induced [Ca2+]i transients in PC3 human prostate cancer cells by stimulating H1 histamine receptors leading to Ca2+ release from the endoplasmic reticulum in an inositol 1,4,5-trisphosphate-dependent manner, and by inducing Ca2+ entry.
Available from: Chung-Yi Chen
- "Neither activation nor inhibition of protein kinase C altered PEITC-induced [Ca 2+ ] i rise. In PC3 cells, thapsigargin/IP 3 -sensitive endoplasmic reticulum Ca 2+ stores are dominant intracellular Ca 2+ stores  . "
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ABSTRACT: The effect of phenethyl isothiocyanate (PEITC), a cruciferous vegetable-derived compound, on cytoplasmic free Ca2+ concentrations ([Ca2+]i) in prostate cells has not been explored. This study examined whether PEITC altered [Ca2+]i levels in suspended human prostate PC3 cancer cells loaded with the Ca2+-sensitive dye fura-2. PEITC caused [Ca2+]i rises in a concentration-dependent manner with an EC50 of 192 μM. Removing extracellular Ca2+ reduced the Ca2+ signal by 42%. PEITC-induced [Ca2+]i rise in Ca2+-containing medium was not affected by modulation of protein kinase C activity, but was inhibited by 90% by the phospholipase A2 inhibitor aristolochic acid (20 μM). In Ca2+-free medium, the PEITC-induced [Ca2+]i rise was changed by depleting store Ca2+ with 1 μM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor). Conversely, PEITC pretreatment abolished thapsigargin-induced [Ca2+]i rise. Chelation of cytosolic Ca2+ with BAPTA did not reverse the decreased cell viability. Collectively, the data suggest that in PC3 cells, PEITC induced a [Ca2+]i increase by causing Ca2+ release from endoplasmic reticulum in a phospholipase A2-dependent fashion and by inducing Ca2+ influx. PEITC decreased cell viability in a concentration-dependent, Ca2+-independent manner. Moreover, the effect of allyl isothiocyanate (AITC), benzyl isothiocyanate (BITC) and PEITC on Ca2+ signaling has also been compared.
Journal of the Taiwan Institute of Chemical Engineers 11/2011; 42(6):895-901. DOI:10.1016/j.jtice.2011.04.009 · 3.00 Impact Factor
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ABSTRACT: The integral equations typically possess singular kernels. Some preliminary analytical regularization is performed before their numerical treatment. The universal and effective direct numerical solution of singular integral equations with the Cauchy type kernels is a well known technique in fracture mechanics. Traditional one-dimensional contour integral equations derived in the scalar diffraction theory are not of such a class. They either possess logarithmic singularity or contain integrals in the finite part sense according to Hadamard. The fields appear during the electromagnetic wave diffraction on the system of cylindrical objects with different properties. Those objects could be perfectly conducting shells and screens, dielectrics, thin absorbed or dielectric films, finite-conducting bodies. Neither the shape of the structure nor cross-section, no position of its elements is bounded by the considered approach. The developed method can be applied in a wide frequency range.
Physics and Engineering of Microwaves, Millimeter, and Submillimeter Waves, 2004. MSMW 04. The Fifth International Kharkov Symposium on; 07/2004
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ABSTRACT: 1. The effect of maprotiline, an antidepressant, on human prostate cells is unclear. In the present study, the effect of maprotiline on [Ca2+]i and growth in PC3 human prostate cancer cells was measured using the fluorescent dyes fura-2 and tetrazolium, respectively.
2. Maprotiline caused a rapid, concentration-dependent increase in [Ca2+]i (EC50 = 200 µmol/L). The maprotiline-induced [Ca2+]i increase was reduced by removal of extracellular Ca2+ or pretreatment with nicardipine.
3. The maprotiline–induced Mn2+ influx-associated fura-2 fluorescence quench directly suggests that maprotiline caused Ca2+ influx.
4. In Ca2+-free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca2+-ATPase, caused a monophasic [Ca2+]i increase, after which the effects of maprotiline of increasing [Ca2+]i were abolished. In addition, pretreatment with maprotiline reduced a major portion of the thapsigargin-induced increase in [Ca2+]i.
5. U73122, an inhibitor of phospholipase C, abolished the ATP (but not maprotiline)-induced increase in [Ca2+]i.
6. Overnight incubation with 1–10 µmol/L maprotiline did not alter cell proliferation, although incubation with 30–50 µmol/L maprotiline decreased cell proliferation.
7, These findings suggest that maprotiline rapidly increases [Ca2+]i in human prostate cancer cells by stimulating both extracellular Ca2+ influx and intracellular Ca2+ release and that it may modulate cell proliferation in a concentration-dependent manner.
Clinical and Experimental Pharmacology and Physiology 08/2004; 31(7):444-9. DOI:10.1111/j.1440-1681.2004.04024.x · 2.37 Impact Factor
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