کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3299741 | 1209935 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Early Growth Response-1 Transcription Factor Is Essential for Ethanol-Induced Fatty Liver Injury in Mice
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کلمات کلیدی
NF-κBcomparative thresholdTLR4LPSEGR-1AP-1ALTROS - ROSAlanine aminotransferase - آلانین آمینوترانسفرازtumor necrosis factor α - تومور نکروز عامل αstandard error of the mean - خطای استاندارد میانگینEMSA یا electrophoretic mobility shift assay - سنجش تغییر تحرک الکتروفورتیکTNF-α - فاکتور نکروز توموری آلفاnuclear factor kappa B - فاکتور هسته ای کاپا Blipopolysaccharide - لیپوپلی ساکاریدSEM - مدل معادلات ساختاری / میکروسکوپ الکترونی روبشیpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازactivator protein-1 - پروتئین فعال کننده-1Reactive oxygen species - گونههای فعال اکسیژنToll-like receptor 4 - گیرنده تله مانند 4
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Early Growth Response-1 Transcription Factor Is Essential for Ethanol-Induced Fatty Liver Injury in Mice Early Growth Response-1 Transcription Factor Is Essential for Ethanol-Induced Fatty Liver Injury in Mice](/preview/png/3299741.png)
چکیده انگلیسی
Background & Aims: Early growth response-1 (Egr-1), an immediate early gene/zinc-finger transcription factor, is required for maximal stimulation of tumor necrosis factor α (TNF-α) transcription in response to lipopolysaccharide (LPS). Because chronic ethanol exposure sensitizes macrophages to LPS-stimulated TNF-α expression, we have investigated the role of Egr-1 in mediating increased LPS-stimulated TNF-α expression after chronic ethanol feeding. Furthermore, because TNF-α contributes to alcoholic liver injury, we tested the hypothesis that Egr-1 is required for the development of ethanol-induced fatty liver injury in wild type and egr-1 â/â mice. Methods: Wild-type and egr-1 â/â mice were fed ethanol-containing diets or pair-fed control diets for 6 weeks. Results: Wild-type mice fed the ethanol diet developed hepatic steatosis characterized by micro- and macrovesicular lipid accumulation. However, egr-1 â/â mice did not develop steatosis after ethanol feeding. Alanine transferase and TNF-α concentrations in serum were increased after ethanol feeding in wild-type but not egr-1 â/â mice. In wild-type mice, challenge with LPS increased Egr-1 messenger RNA (mRNA) and DNA binding activity in liver; this response to LPS was enhanced after chronic ethanol feeding. LPS challenge also increased hepatic TNF-α mRNA and serum TNF-α to a greater extent after ethanol feeding compared with pair-fed wild-type mice. However, chronic ethanol feeding did not enhance LPS-stimulated TNF-α mRNA or serum TNF-α in egr-1 â/â mice. Conclusions: These data show that Egr-1 contributes to increased LPS-mediated TNF-α expression after chronic ethanol and that the absence of Egr-1 prevents chronic ethanol-induced fatty liver, as well as increased sensitivity to LPS.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 128, Issue 7, June 2005, Pages 2066-2076
Journal: Gastroenterology - Volume 128, Issue 7, June 2005, Pages 2066-2076
نویسندگان
Megan R. McMullen, Michele T. Pritchard, Qifang Wang, Carrie A. Millward, Colleen M. Croniger, Laura E. Nagy,