کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8268109 | 1534951 | 2016 | 50 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Glyoxalase I drives epithelial-to-mesenchymal transition via argpyrimidine-modified Hsp70, miR-21 and SMAD signalling in human bronchial cells BEAS-2B chronically exposed to crystalline silica Min-U-Sil 5: Transformation into a neoplastic-like phenotype
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کلمات کلیدی
TRITCRIPAAP-1PMSFBPEDAPIAGEsTBSTc-Jun NH2-terminal kinaseCATZO-1miRNAsSMADsJnkGLO1TGF-β1tris-buffered saline tween 20phenylmethanesulphonylfluorideα-SMATetramethylrhodamine B isothiocyanate4′,6-diamidino-2-phenylindole - 4 '، 6-دیامیدینو-2-فنیلینولBMPs - BMP هاE-cad - E-CADE-cadherin - E-CadherinGSH-Px - GSH-PXROS - ROSHydrogen peroxide - آب اکسیژنهAminoguanidine - آمینوگوئیدینInternational Agency for Research on Cancer - آژانس بین المللی تحقیقات سرطانIARC یا International Agency for Research on Cancer - آژانس بین المللی تحقیقات سرطانArgpyrimidine - ارگپیریمیدینepithelial to mesenchymal transition - اپیتلیال به انتقال مزانشیمالα-smooth muscle actin - اکتین عضله آلفا صافmiR-21 - به miR-21transforming growth factor beta 1 - تبدیل فاکتور رشد بتا 1EMT - تکنسین فوریتهای پزشکیmicroRNAs - ریز آرانایSOD - سدradioimmunoprecipitation assay - سنجش radioimmunoprecipitationSuperoxide dismutase - سوکسوکس دیسموتازbovine pituitary extract - عصاره هیپوفیز گاوMethylglyoxal - متیل گلی اکسالAdvanced glycation end products - محصولات نهایی پیشرفته گلیساسیونZonula occludens-1 - نوار ابزار بسته 1H2O2 - هیدروژن پراکسیدactivator protein-1 - پروتئین فعال کننده-1bone morphogenetic proteins - پروتئین های مورفوژنیک استخوانCatalase - کاتالازglutathione peroxidase - گلوتاتیون پراکسیدازglyoxalase I - گلیوکسیلاز IReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Glyoxalase I (Glo1) is the main scavenging enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs). AGEs are known to control multiple biological processes, including epithelial to mesenchymal transition (EMT), a multistep phenomenon associated with cell transformation, playing a major role in a variety of diseases, including cancer. Crystalline silica is a well-known occupational health hazard, responsible for a great number of human pulmonary diseases, such as silicosis. There is still much debate concerning the carcinogenic role of crystalline silica, mainly due to the lack of a causal demonstration between silica exposure and carcinogenesis. It has been suggested that EMT might play a role in crystalline silica-induced lung neoplastic transformation. The aim of this study was to investigate whether, and by means of which mechanism, the antiglycation defence Glo1 is involved in Min-U-Sil 5 (MS5) crystalline silica-induced EMT in BEAS-2B human bronchial epithelial cells chronically exposed, and whether this is associated with the beginning of a neoplastic-like transformation process. By using gene silencing/overexpression and scavenging/inhibitory agents, we demonstrated that MS5 induced hydrogen peroxide-mediated c-Jun-dependent Glo1 up-regulation which resulted in a decrease in the Argpyrimidine-modified Hsp70 protein level which triggered EMT in a novel mechanism involving miR-21 and SMAD signalling. The observed EMT was associated with a neoplastic-like phenotype. The results obtained provide a causal in vitro demonstration of the MS5 pro-carcinogenic transforming role and more importantly they provide new insights into the mechanisms involved in this process, thus opening new paths in research concerning the in vivo study of the carcinogenic potential of crystalline silica.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 92, March 2016, Pages 110-125
Journal: Free Radical Biology and Medicine - Volume 92, March 2016, Pages 110-125
نویسندگان
Cinzia Antognelli, Angela Gambelunghe, Giacomo Muzi, Vincenzo Nicola Talesa,