کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9001900 | 1118561 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Role of Ca2+-independent phospholipase A2 and cytochrome P-450 in store-operated calcium entry in 3T6 fibroblasts
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کلمات کلیدی
CCEcalcium influx factorAACOCF3intracellular calcium concentrationsInsP3iPLA2CIFPLA2BELFCSCRAC[Ca2+]i - [Ca2 +] iphospholipase A2 - آنزیم فسفولیپاز A2 Arachidonic acid - اسید آراشیدونیکepoxyeicosatrienoic acids - اسید اپوکسی اسیاتریتروئینepoxyeicosatrienoic acid - اسید اپوکسی اسیاتریتروئینeicosanoids - ایکوزانوئیدها bromoenol lactone - بروموآنول لاکتونEET - خوردنfetal calf serum - سرم گوساله جنینSOC - سیستم روی یک تراشهendoplasmic reticulum - شبکه آندوپلاسمی calcium-independent phospholipase A2 - فسفولیپاز A2 مستقل از کلسیم استArc - قوسCapacitative calcium entry - ورودی کافی از کلسیمCalcium channels - کانال های کلسیم
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Role of Ca2+-independent phospholipase A2 and cytochrome P-450 in store-operated calcium entry in 3T6 fibroblasts Role of Ca2+-independent phospholipase A2 and cytochrome P-450 in store-operated calcium entry in 3T6 fibroblasts](/preview/png/9001900.png)
چکیده انگلیسی
Store-operated calcium (SOC) channels and capacitative Ca2+ entry play a key role in cellular functions, but their mechanism of activation remains unclear. Here, we show that thapsigargin induces [3H] arachidonic acid (AA) release, 45Ca2+ influx and a subsequent enhancement of intracellular calcium concentration ([Ca2+]i. Thapsigargin-induced elevation of [Ca2+]i was inhibited by cytochrome P-450 inhibitors and by cytochrome P-450 epoxygenase inhibitor and was reverted by 11,12 EET addition. However, cyclooxygenase and lipoxygenase inhibitors have no effect. Moreover, we observed that four EETs were able to induce 45Ca2+ influx. Finally, we reported that the effect of 11,12 EET on 45Ca2+ influx was sensible to receptor-operated Ca2+ channel blockers (NiCl2, LaCl3) but not to voltage-dependent Ca2+ channel blocker as verapamil. Thus, AA released by Ca2+-independent phospholipase A2 and AA metabolism through cytochrome P-450 pathway may be crucial molecular determinant in thapsigargin activation of SOC channels and store-operated Ca2+ entry pathway in 3T6 fibroblasts. Moreover, EETs, the main cytochrome P-450 epoxygenase metabolites of AA, are involved in thapsigargin-stimulated Ca2+ influx. In summary, our results suggest that EETs are components of calcium influx factor(s).
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical Pharmacology - Volume 70, Issue 5, 1 September 2005, Pages 733-739
Journal: Biochemical Pharmacology - Volume 70, Issue 5, 1 September 2005, Pages 733-739
نویسندگان
Javier MartÃnez, Juan J. Moreno,