کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8322024 | 1539844 | 2018 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hepatitis B virus X protein and proinflammatory cytokines synergize to enhance TRAIL-induced apoptosis of renal tubular cells by upregulation of DR4
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Hepatitis B virus X protein and proinflammatory cytokines synergize to enhance TRAIL-induced apoptosis of renal tubular cells by upregulation of DR4 Hepatitis B virus X protein and proinflammatory cytokines synergize to enhance TRAIL-induced apoptosis of renal tubular cells by upregulation of DR4](/preview/png/8322024.png)
چکیده انگلیسی
Persistent infection with hepatitis B virus (HBV) may lead to HBV-associated glomerulonephritis (HBV-GN). Presence of HBV-DNA and -RNA in renal tubular epithelial cells (RTECs) suggests direct virus-induced injury. Increase in proinflammatory cytokines is also observed under these conditions. Apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) plays a significant role in the pathogenesis of HBV-infections. However, the effects of HBV X protein (HBx) on TRAIL-induced apoptosis of RTECs especially under certain inflammatory conditions remain obscure. Here, we show that HBx synergizes with proinflammatory cytokines to significantly increase TRAIL-induced apoptosis of RTECs. HBx markedly up-regulates death receptor-4 (DR4) expression by enhancing the activation of nuclear factor-kappa B (NF-κB) in the presence of proinflammatory cytokines. Dramatic increase in DR4 expression leads to the sensitization of RTECs to TRAIL-induced apoptosis. Furthermore, in patients with HBV-GN, DR4 expression in the kidneys is significantly elevated and is positively correlated with the HBx and proinflammatory cytokines expression. These findings provide a novel insight into the underlying mechanisms of renal tubule lesions induced by HBx in HBV-GN.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 97, April 2018, Pages 62-72
Journal: The International Journal of Biochemistry & Cell Biology - Volume 97, April 2018, Pages 62-72
نویسندگان
Yitong Yang, Xuan Wang, Yueyue Zhang, Weijie Yuan,