کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1911163 | 1046804 | 2008 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Glutamate cysteine ligase up-regulation fails in necrotizing pancreatitis
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
NF-κBRNaseCBPGSHAP-1ERKGCLAIDS - ایدزchromatin immunoprecipitation - ایمن سازی کروماتینanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceFree radicals - رادیکال آزادribonuclease - ریبونوکلئازacquired immune deficiency syndrome - سندروم نقص ایمنی اکتسابیnuclear factor κB - فاکتور هسته ای κBglutamate cysteine ligase - لیگاز سیتئین گلوتاماتNecrosis - نکروز یا بافتمردگیpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازAcute pancreatitis - پانکراتیت حادactivator protein-1 - پروتئین فعال کننده-1CHiP - چیپreduced glutathione - کاهش گلوتاتیونextracellular regulated kinase - کیناز تنظیم شده خارج سلولیGlutathione - گلوتاتیون
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Glutamate cysteine ligase up-regulation fails in necrotizing pancreatitis Glutamate cysteine ligase up-regulation fails in necrotizing pancreatitis](/preview/png/1911163.png)
چکیده انگلیسی
Glutathione depletion is a key factor in the development of acute pancreatitis. Our aim was to study the regulation of glutamate cysteine ligase, the rate-limiting enzyme in glutathione synthesis, in edematous or necrotizing pancreatitis in rats. Glutathione levels were kept low in necrotizing pancreatitis for several hours, with no increase in protein or mRNA levels of glutamate cysteine ligase subunits, despite binding of RNA polymerase II to their promoters and coding regions. The survival signal pathway mediated by ERK and c-MYC was activated, and c-MYC was recruited to the promoters. The failure in gene up-regulation seems to be due to a marked increase in cytosolic ribonuclease activity. In contrast, in edematous pancreatitis glutathione levels were depleted and rapidly restored, and protein and mRNA expression of glutamate cysteine ligase increased markedly due to enhanced transcription mediated by recruitment of c-MYC, NF-κB, and SP-1 to the promoters. No increase in cytosolic ribonuclease activity was found in this case. We propose a novel pathophysiological mechanism to differentiate necrotizing from edematous pancreatitis, which is the inefficient up-regulation of glutamate cysteine ligase caused by increased cytosolic ribonuclease activity in the severe form of the disease. This mechanism would abrogate a rapid recovery of glutathione levels.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 44, Issue 8, 15 April 2008, Pages 1599-1609
Journal: Free Radical Biology and Medicine - Volume 44, Issue 8, 15 April 2008, Pages 1599-1609
نویسندگان
Javier Pereda, Javier Escobar, Juan Sandoval, José Luis RodrÃguez, Luis Sabater, Federico V. Pallardó, Luis Torres, Luis Franco, José Viña, Gerardo López-Rodas, Juan Sastre,