Hepatitis B virus X protein and proinflammatory cytokines synergize to enhance TRAIL-induced apoptosis of renal tubular cells by upregulation of DR4

Yang, Yitong; Wang, Xuan; Zhang, Yueyue; Wang, Yuan

doi:10.1016/j.biocel.2018.02.006

Cited by 13 publications

(14 citation statements)

References 42 publications

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“…In our previous study, IHC analysis in the renal biopsies showed that the expression of tumor necrosis factor-alpha (TNF-α) was increased in HBV-GN 35 . In the present study, IHC analysis in the renal biopsies also showed that the expression of other inflammatory markers, including interleukin (IL)-1β, IL-6, monocyte chemoattractant protein-1 (MCP-1), and CD68 (macrophage marker), was markedly increased in HBV-GN than in non-HBV-GN (Fig.…”

Section: Resultsmentioning

confidence: 96%

“…NF-κB, an inflammatory transcription factor, has an important role in the pathogenesis of HBV-associated nephropathy 35,48 . NF-κB activation is triggered by p65 phosphorylation and IκB phosphorylation and subsequent degradation, which causes NF-κB translocation to the nucleus and subsequent transcription of several target genes 49 .…”

Section: Discussionmentioning

confidence: 99%

“…ChIP assay was performed using the SimpleCHIP enzymatic chromatin immunoprecipitation kit (Cell Signaling Technology, MA, USA) as described previously 35 . After treatment, the cells were harvested and crosslinked with 1% (v/v) formaldehyde for 10 min at RT.…”

Section: Methodsmentioning

confidence: 99%

“…Briefly, the pGL3-TLR4-wt and pGL3-TLR4-mut plasmids were separately co-transfected with the pRL-TK renilla vector using Lipofectamine 3000 (Invitrogen). Twelve hours after transfection, cells were co-transfected with pCMV-HBV1.3 and LSD1 shRNAs for another 24 h. Cells were harvested, and luciferase activity was measured as described previously 35 . The ratio of firefly luciferase to renilla luciferase was calculated in each group.…”

Section: Methodsmentioning

confidence: 99%

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The histone demethylase LSD1 promotes renal inflammation by mediating TLR4 signaling in hepatitis B virus-associated glomerulonephritis

et al. 2019

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Renal inflammation significantly contributes to the progression of hepatitis B virus (HBV)-associated glomerulonephritis (HBV-GN), but the mechanisms that control its precise regulation remain largely unknown. In this study, we showed that the lysine-specific demethylase 1 (LSD1) was significantly upregulated in renal tissue of HBV-GN patients, and its expression was positively correlated with inflammation. Functionally, LSD1 could promote HBV-induced release of proinflammatory mediators in HK-2 cells, a human renal tubular epithelial (RTE) cell line. Mechanistic investigations suggested that LSD1 directly promoted the transcription of the inflammatory-related gene Tlr4 by eliminating the mono- or di-methylation of H3K9 near its promoter. Knockdown of Lsd1 further inhibited TLR4-NF-κB/JNK signaling cascades, and subsequently decreased HBV-induced production of proinflammatory mediators in HK-2 cells. Co-transfection with Tlr4-expressing plasmids counteracted these effects. Meanwhile, downregulation of abovementioned TLR4-related pathways using small-molecule inhibitors attenuated inflammation. Importantly, LSD1 inhibitor tranylcypromine (TCP) could inhibit TLR4-NF-κB/JNK signaling axis and alleviate renal inflammation in HBV transgenic mice. Taken together, our data identify LSD1 as a novel regulator of renal inflammation and as a potential therapeutic target in HBV-GN.

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Section: Resultsmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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The histone demethylase LSD1 promotes renal inflammation by mediating TLR4 signaling in hepatitis B virus-associated glomerulonephritis

et al. 2019

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“…Except for glomerular immune complexes depositing from circulating immune complexes and/or form in situ, HBV virus may directly infect glomerular cells contributing to the pathogenesis of HBV-GN. 26 Therefore, the mechanism of HBsAg+ HBV-GN may be more complicated, resulting in diversity of histologic manifestations.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B Virus-Related Glomerulonephritis with Positive and Negative Serum HBsAg: Different Clinicopathologic Characteristics of Two Clinical Subtypes

Yu¹,

Li²,

Hao³

et al. 2021

IJGM

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Introduction The clinicopathologic characteristics of Hepatitis B virus-associated glomerulonephritis (HBV-GN) patients with different serum HBsAg are not well known. This study aims to investigate the characteristics and treatments between HBV-GN patients with positive and negative serum HBsAg. Methods A retrospective review of patients with renal biopsies in Guangdong Provincial People’s Hospital from 2005 to 2018 was performed. Clinicopathological data, treatments and remission of proteinuria were collected and compared between HBsAg+ and HBsAg- group. Results A total of 101 HBV-GN were recruited. Serum HBsAg+ and HBsAg- patients accounted for 62.4% and 37.6%, respectively. HBsAg+ group had poor kidney and liver functions. Pathological data showed the percentage of membranous nephropathy in HBsAg- group is significantly higher than that of HBsAg+ group (60.3% HBsAg+ vs 89.5% HBsAg-, P <0.05). Chronic renal tubular/interstitial injury was more prevalent in HBsAg+ group (16.9% HBsAg+ vs 2.6% HBsAg-, P <0.05). The deposition sites of immune complexes were significant different between the two groups. In addition, more HBsAg+ patients were given anti-HBV and less were given corticosteroid or immunosuppressants for treatment than that of HBsAg- patients. Percentages of clinical remission were increasing in both HBsAg+ and HBsAg- patients from 1, 3, 6 months to 1 year (18.75%, 45.2%, 67.8%, 82.4% vs 24.4%, 41.2%, 62.8%, 59.3%). The differences of remission betwen two groups were not significant ( P >0.05). Conclusion The clinicopathological characteristics and treatments of HBV-GN with serum HBsAg+ and HBsAg- were distinct, which indicated that the pathogenesis might be different and specific treatments were needed for HBV-GN patients with different serum HBsAg.

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Cytokines and chemokines involved in the defense reaction against HIV-1 and hepatitis B virus: isn’t it time to use a standardized nomenclature of the involved mediators?

Gürtler

2019

Virus Genes

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Hepatitis B virus X protein and proinflammatory cytokines synergize to enhance TRAIL-induced apoptosis of renal tubular cells by upregulation of DR4

Cited by 13 publications

References 42 publications

The histone demethylase LSD1 promotes renal inflammation by mediating TLR4 signaling in hepatitis B virus-associated glomerulonephritis

The histone demethylase LSD1 promotes renal inflammation by mediating TLR4 signaling in hepatitis B virus-associated glomerulonephritis

Hepatitis B Virus-Related Glomerulonephritis with Positive and Negative Serum HBsAg: Different Clinicopathologic Characteristics of Two Clinical Subtypes

Cytokines and chemokines involved in the defense reaction against HIV-1 and hepatitis B virus: isn’t it time to use a standardized nomenclature of the involved mediators?

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