کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
9894085 1542260 2005 16 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The effect of prostaglandin E1 on ion currents of NG108-15 cells
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
The effect of prostaglandin E1 on ion currents of NG108-15 cells
چکیده انگلیسی
The aim of this study was to elucidate the mechanism by which prostaglandin E1 (PGE1) acts on ion currents of whole-cell voltage-clamped NG108-15 neuroblastoma × glioma hybrid cells. Ruptured and perforated patch were used. The holding current at −70 mV, the current-voltage curve produced by ramp pulses from −70 to 0 mV and the T-type and hva (high-voltage-activated) Ca2+ currents associated with rectangular pulses were recorded. Bath application of PGE1 (0.2 or 3 μM) reversibly increased the holding current, an effect mimicked by the prostanoid agonist iloprost (5-50 nM). The PGE1 effect was totally blocked by the cAMP-antagonist Rp-cAMPS whereas H-89, an inhibitor of protein kinase A (PKA), failed to inhibit it, even when applied in the fairly high bath concentration of 30 μM. PGE1 and iloprost also inhibited the T-type and hva Ca2+ currents and this effect of PGE1 was likewise not prevented by H-89. In some of the cells, the PGE1 effect on holding current could be mimicked by 8-pCPT-2Me-cAMP (100-300 μM), a selective agonist of Epac (exchange protein activated by cAMP), but unlike the PGE1 effect its action was not abolished by Rp-cAMPS. The effect of PGE1 on the the holding current and on the T-type Ca2+ current was diminished when EGTA in the pipette solution was replaced by BAPTA, suggesting that Ca2+ ions are involved in the PGE1 effect. It is concluded that the PGE1 effect is mediated by cAMP and Ca2+ ions but not by PKA or Epac.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Prostaglandins & Other Lipid Mediators - Volume 76, Issues 1–4, May 2005, Pages 117-132
نویسندگان
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