کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9245502 | 1209948 | 2005 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Bile acids induce hepatic stellate cell proliferation via activation of the epidermal growth factor receptor
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
ERKGCDCAPCNATGFPKCEGFRmTORJnkEGFPI3KMMPHSCc-Jun N-terminal kinase - C-Jun N-terminal kinaseProliferating Cell Nuclear Antigen - آنتیژن هسته ای تکثیر سلولیsmooth muscle actin - آکنه عضله صافGlycochenodeoxycholic acid - اسید گلیکوزید سدیم اسیدBrdU - بروموداکسی اوریدینbromodeoxyuridine - برومودسوویریدینSMA - دبیرستانHepatic stellate cell - سلول ستاره ای کبدیepidermal growth factor - عامل رشد اپیدرمیPhosphatidylinositol 3-kinase - فسفاتیدیلینواستیل 3-کینازMatrix metalloprotease - ماتریکس متیل پروتئازایMEK - مجاهدین خلقmammalian target of rapamycin - هدف پستانداران رپامایسینpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازProtein kinase C - پروتئین کیناز سیmitogen-activated protein kinase kinase - پروتئین کیناز کیناز فعال Mitogen فعالextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیEpidermal growth factor receptor - گیرنده فاکتور رشد اپیدرمال
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Background & Aims: Hepatic stellate cell (HSC) proliferation is a key event in the development of liver fibrosis. In many liver diseases, HSCs are exposed to inflammatory cytokines, reactive oxygen species, and bile acids. Although inflammatory cytokines and reactive oxygen species are known to promote proliferation of HSCs, nothing is known about the effects of bile acids on HSC proliferation or apoptosis. The aim of this study was to investigate the effects of bile acids on HSC proliferation. Methods: HSCs were exposed to bile acids with different hydrophobicity (5-200 μmol/L). HSC proliferation and cell cycle-related events were assessed by bromodeoxyuridine incorporation, cell counting and proliferating cell nuclear antigen and cyclin E expression, apoptosis by caspase-3 activity assay, immunocytochemistry for active caspase-3 and acridine orange staining, and activation of signal transduction pathways by Western blot using phospho-specific antibodies. Uptake of bile acids was investigated using fluorescent bile acids. Results: All bile acids, at concentrations >25 μmol/L, induce a 2.5- to 3-fold increase in HSC proliferation via activation of the epidermal growth factor receptor. Bile acid-induced proliferation is mediated by activation of a protein kinase C/extracellular signal-regulated kinase/p70S6K-dependent pathway. Bile acids did not induce apoptosis in HSCs. HSCs do not take up fluorescent bile acids and do not express the bile acid importer ntcp. Conclusions: Bile acids at levels reached in cholestatic conditions are an independent profibrogenic factor. Bile acids induce HSC proliferation via the activation of the epidermal growth factor receptor, whereas HSCs are protected against bile acid-induced apoptosis by excluding bile acids.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 128, Issue 4, April 2005, Pages 1042-1055
Journal: Gastroenterology - Volume 128, Issue 4, April 2005, Pages 1042-1055
نویسندگان
Gianluca Svegliati-Baroni, Francesco Ridolfi, Rebekka Hannivoort, Stefania Saccomanno, Manon Homan, Samuele de Minicis, Peter L.M. Jansen, Cinzia Candelaresi, Antonio Benedetti, Han Moshage,