کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9002131 | 1118574 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
2-Aminoethoxydiphenyl borate perturbs hormone-sensitive calcium stores and blocks store-operated calcium influx pathways independent of cytoskeletal disruption in human A549 lung cancer cells
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کلمات کلیدی
sarcoplasmic/endoplasmic reticulum Ca2+-ATPaseHBSSIP32-aminoethoxydiphenyl borateThapsigarginIP3RCCCP2-APBinositol 1,4,5-trisphosphate - inositol 1،4،5-trisphosphate[Ca2+]i - [Ca2 +] iIntracellular Ca2+ - داخل سلولی Ca2 +SOC - سیستم روی یک تراشهendoplasmic reticulum - شبکه آندوپلاسمی Calcium stores - فروشگاه های کلسیمSERCA - قلبHank's balanced salt solution - محلول نمک متعادل هانکStore-operated calcium influx - ورودی کلسیم با استفاده از فروشگاهCytoskeleton - چارچوب یاخته، سیتواسکلتون، اسکلت سلولیStore-operated Ca2+ channel - کانال Ca2 + ذخیره شدهCarbonyl cyanide 3-chlorophenylhydrazone - کربنیل سیانید 3-کلروفنیل هیدرازونInositol 1,4,5-trisphosphate receptor - گیرنده inositol 1،4،5-trisphosphate
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
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چکیده انگلیسی
Recent studies have identified novel actions for 2-aminoethoxydiphenyl borate (2-APB) in triggering calcium release and enhancing calcium influx induced by the depletion of intracellular calcium stores. In this study, we have examined the effects of 2-APB on the human lung adenocarcinoma A549 cell line, which we have previously shown displays a unique calcium influx response, when ER calcium stores are depleted by thapsigargin (TG) treatment. Here, we show that low concentrations of 2-APB failed to induce the rapid augmentation of TG-activated calcium influx previously reported for other cell types. We observed that store-operated calcium (SOC) channels in the A549 cell line exhibited short-term sensitivity to low doses of 2-APB, perhaps reflecting a delayed augmentation of SOC channel activity or the recruitment of 2-APB-insensitive SOC channels. In both intact and permeabilized cells, 2-APB effectively discharged a subset of A549 calcium pools corresponding to the hormone-sensitive intracellular calcium stores. The 2-APB-induced calcium release produced a long-lasting perturbation of the adenosine triphosphate (ATP)-releasable calcium pools, effectively uncoupling ATP-activated calcium release even, when stores are replenished with calcium. In contrast to previous reports, we found that disruption of either the actin or microtubule-based cytoskeleton failed to block the 2-APB-induced effects on calcium signaling in A549 cells. Our study describes novel cytoskeletal-independent effects of 2-APB on Ca2+-signaling pathways, revealing differentially sensitive Ca2+-influx pathways and long-term perturbation of hormone-sensitive Ca2+ stores.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical Pharmacology - Volume 69, Issue 8, 15 April 2005, Pages 1177-1186
Journal: Biochemical Pharmacology - Volume 69, Issue 8, 15 April 2005, Pages 1177-1186
نویسندگان
Shanthala Padar, Diptiman D. Bose, John C. Livesey, David W. Thomas,