کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8962159 | 1646544 | 2018 | 39 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hepatitis B virus upregulates host microRNAs that target apoptosis-regulatory genes in an in vitro cell model
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کلمات کلیدی
HBSsilencer of death domainsSODDmiR-194HBV X proteincellular FLICE-inhibitory proteincFLIPCHBHBxThapsigarginHepG2HCC - HCCmitochondrial outer membrane permeabilization - permeabilization غشای خارجی بیرونی میتوکندریNon-coding RNA - RNA غیرکد کننده، RNA غیرترجمه شوندهtumor necrosis factor alpha - تومور نکروز عامل آلفاApoptosis - خزان یاختهایendoplasmic reticulum - شبکه آندوپلاسمی TNF-α - فاکتور نکروز توموری آلفاMOMP - ماموریتchronic hepatitis B - هپاتیت B مزمن، هپاتیت ب مزمنHBV - هپاتیت بhepatitis B virus - ویروس هپاتیت بیHepatocellular carcinoma - کارسینوم هپاتوسلولار(کارسینوم سلولهای استخوانی)
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Chronic hepatitis B (CHB) infection increases the risk of developing severe liver disease including cirrhosis and hepatocellular carcinoma (HCC). As microRNAs may modulate host - virus interactions, we here investigated if hepatitis B virus (HBV) infection modulate microRNA expression using an in vitro HepG2 cell model system with inducible HBV replication. We found that HBV replication was associated with upregulation of miR-192-5p, miR-194-5p and miR-215-5p, of which miR-192-5p and miR-215-5p have identical seed sequences. Bioinformatics analyses revealed a significant enrichment of potential target genes involved in apoptosis signaling of all three microRNAs. In line with this, transfection with a mimic of miR-192-5p suppressed the protein level of pro-apoptotic BIM and reduced endoplasmic reticulum (ER) stress-induced apoptosis in HepG2 cells. In contrast, transfection with a mimic of miR-194-5p downregulated the anti-apoptotic proteins SODD and cFLIP, and sensitized HepG2 cells to both ER stress- and cytokine-induced apoptosis. In conclusion, our study suggests that HBV upregulates the expression of miR-192-5p and miR-194-5p in the host cell. These microRNAs target important apoptosis-regulatory proteins, and may thus contribute to the development of HBV-related liver disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 371, Issue 1, 1 October 2018, Pages 92-103
Journal: Experimental Cell Research - Volume 371, Issue 1, 1 October 2018, Pages 92-103
نویسندگان
Kirstine Overgaard Nielsen, Kari Stougaard Jacobsen, Aashiq Hussain Mirza, Thilde Nordmann Winther, Joachim Størling, Dieter Glebe, Flemming Pociot, Birthe Hogh,