کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9001631 | 1118539 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Distinct effects of N-ethylmaleimide on formyl peptide- and cyclopiazonic acid-induced Ca2+ signals through thiol modification in neutrophils
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کلمات کلیدی
CPAtris-(2-carboxyethyl)phosphinesarcoplasmic-endoplasmic reticulum Ca2+-ATPaseROCEformyl-met-leu-phefMLPFPRSOCEIP3RPLCIP3N-acetyl-l-cysteineInositol trisphosphateTrpN-ethylmaleimideNACRT-PCRDTNBHBSS5,5′-dithiobis-2-nitrobenzoic acid - 5،5'-dithiobis-2-nitrobenzoic acidCa2+ release - آزادی Ca2 +Cyclopiazonic acid - اسید سیکلوپیاازونیکTCEP - ساکتphospholipase C - فسفولیپاز CTCP - قرارداد هدایت انتقالSERCA - قلبHanks’ balanced salt solution - محلول نمک متعادل هانکسNEM - نهNeutrophils - نوتروفیل هاreverse transcription-polymerase chain reaction - واکنش زنجیره ای رونویسی-پلیمراز معکوسCa2+ entry - ورودی Ca2 +Store-operated Ca2+ entry - ورودی Ca2 + ذخیره شدهtransient receptor potential - پتانسیل گیرنده گذراInositol trisphosphate receptor - گیرنده inositol trisphosphateformyl peptide receptor - گیرنده پپتید فرمولی
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
In this study, we demonstrate that N-ethylmaleimide (NEM), a cell permeable thiol-alkylating agent, enhanced the [Ca2+]i rise caused by stimulation with cyclopiazonic acid (CPA), a sarcoplasmic-endoplasmic reticulum Ca2+-ATPase inhibitor, in rat neutrophils. In addition, NEM attenuated the formyl-Met-Leu-Phe (fMLP)-induced [Ca2+]i rise whether NEM was added to cells prior to or after fMLP stimulation. Moreover, application of NEM after fMLP activation in the absence of external Ca2+ inhibited the Ca2+ signal upon addition of Ca2+ to the medium. Similar patterns were also obtained by using 5,5â²-dithiobis-(2-nitrobenzoic acid) (DTNB), a cell impermeable dithiol-oxidizing agent, which replaced NEM in the CPA- and fMLP-induced [Ca2+]i rise experiments. Treatment with dithiothreitol (DTT), a cell permeable dithiol-reducing agent, N-acetyl-l-cysteine (NAC), a cell permeable monothiol-reducing agent, and tris-(2-carboxyethyl)phosphine (TCEP), a cell impermeable reductant without a thiol group, all rescued the fMLP-induced Ca2+ signal from NEM. Rat neutrophils express the mRNA encoding for transient receptor potential (TRP) C6, inositol trisphosphate receptor (IP3R) 2 and IP3R3. NEM had no effect on the mitochondrial membrane potential. NEM could restore the polarization and F-actin accumulation of fMLP-treated cells to those of the control. In the absence of external Ca2+, NEM rendered the CPA-induced [Ca2+]i elevation persistently but inhibited the fMLP-induced Ca2+ spike, which was reversed by tris-(2-cyanoethyl)phosphine (TCP), a cell permeable reductant without a thiol group. DTNB did not affect the Ca2+ spike caused by fMLP. These results indicate that through protein thiol oxidation, NEM affects the receptor-activated and the store depletion-derived Ca2+ signals in an opposing manner.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical Pharmacology - Volume 70, Issue 9, 1 November 2005, Pages 1320-1329
Journal: Biochemical Pharmacology - Volume 70, Issue 9, 1 November 2005, Pages 1320-1329
نویسندگان
Mei-Feng Hsu, Shu-Ping Sun, Yu-San Chen, Chi-Ren Tsai, Li-Jiau Huang, Lo-Ti Tsao, Sheng-Chu Kuo, Jih-Pyang Wang,