کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2602757 | 1133797 | 2010 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Manganese-mediated up-regulation of HIF-1α protein in Hep2 human laryngeal epithelial cells via activation of the family of MAPKs
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کلمات کلیدی
iNOSPKBHRECHXHIF-1αVHLIGF-1ECLIL-1βHIF-1βIκB-αinhibitory kappa B-αCOX-2GAPDHATF-2PKC-αERK-1/2Hep2 cellsFBSTGF-β1protein kinase C-αMAPK - MAPKp38 MAPK - P38 MAPKVon Hippel–Lindau - از Hippel-Lindauinsulin-like growth factor-1 - انسولین مانند عامل رشد 1Interleukin-1β - اینترلوکین-1βTransforming growth factor-β1 - تبدیل فاکتور رشد β1fetal bovine serum - سرم جنین گاوinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییcycloheximide - سیکلوهایسیمیدCyclooxygenase-2 - سیکلوکوکسیژناز2hypoxia inducible factor-1α - عامل القایی هیپوکسی 1αHypoxia responsive element - عنصر پاسخگو هیپوکسیVascular endothelial growth factor - فاکتور رشد اندوتلیال عروقیVascular Endothelial Growth Factor (VEGF) - فاکتور رشد اندوتلیال عروقی (VEGF)activating transcription factor-2 - فعال کردن عامل رونویسی 2Manganese - منگنز protein kinase B - پروتئین کیناز Bmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenglyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
High exposure of manganese is believed to be a risk factor for respiratory diseases. Evidence suggests that overexpression of HIF-1α transcription factor is linked to pulmonary inflammation and vascular change. In this study, we investigated the effect of manganese-chloride (manganese) on expression and activity of HIF-1α in various human airway cells, including Hep2 (laryngeal), H292 (bronchial), and A549 (lung). Profoundly, while manganese treatment led to low or little effect on induction of HIF-1α protein in H292 or A549 cells, it strongly induced HIF-1α protein expression in Hep2 cells. Mn treatment, however, did not induce HIF-1α mRNA expression in Hep2 cells. Luciferase experiments further demonstrated that manganese treatment increased the HRE-driven luciferase activity, suggesting that the induced HIF-1 is functional. Interestingly, manganese treatment also caused activation of p38 MAPK, JNK-1/2, ERK-1/2, and ATF-2, but not of PKB or NF-κB in Hep2 cells. Importantly, the manganese-mediated expression and activity of HIF-1α protein were largely blocked by treatment with the inhibitor of p38 MAPK (SB203580), JNK-1/2 (SP600125), or ERK-1/2 (PD98059), suggesting roles of these MAPKs in the manganese-induced HIF-1α protein expression and activity. Moreover, treatment with SP600125 or SB203580, but not PD98059, had partial inhibitory effects on the stability of HIF-1α protein induced by manganese, suggesting that p38 MAPK and JNK-1/2 also contribute to the Mn-mediated HIF-1α protein stability. These results suggest that manganese is able to up-regulate HIF-1α at the protein level in Hep2 cells and the up-regulation is largely dependent of activities of the family of MAPKs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology in Vitro - Volume 24, Issue 4, June 2010, Pages 1208-1214
Journal: Toxicology in Vitro - Volume 24, Issue 4, June 2010, Pages 1208-1214
نویسندگان
Hee-Jung Shin, Mi-Sun Choi, Nam-Hee Ryoo, Ki-Young Nam, Gy-Young Park, Jae-Hoon Bae, Seong-il Suh, Won-Ki Baek, Jong-Wook Park, Byeong-Churl Jang,