A role for MHBst167/HBx in hepatitis B virus-induced renal tubular cell apoptosis
Abstract
The pathogenesis of hepatitis B virus (HBV)-associated glomerulonephritis (HBVGN) is generally believed to be immune complex deposition. However, the presence of HBV-DNA and -RNA in HBVGN renal tissues suggested a direct virally induced injury. We previously showed that nuclear factor kappaB (NF-kappaB) was activated in HBVGN renal tissues, especially in tubular cells. We therefore investigated the role of NF-kappaB in tubular epithelial cells with HBV infection. Nuclear translocation of NF-kappaB and alpha subunit of NF-kappaB inhibitor (IkappaBalpha) phosphorylation were assessed by immunodetection following transfection of HK-2 cells with mhbs(t167) and/or hbx. Electrophoretic mobility shift assays (EMSA) and dual luciferase reporter assays (DLR) were used to further examine NF-kappaB activation following transfection. Hochest 33258 and NF-kappaB/terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) double staining were used to detect apoptosis and the correlation between NF-kappaB activation and apoptosis. Protein kinase C (PKC) assay and ERK phosphorylation were assayed for a possible mechanism of NF-kappaB activation. Cells transfected with mhbs(t167) and/or hbx increased NF-kappaB nuclear translocation, ph...Continue Reading
References
Hepatitis B infection and renal disease: clinical, immunopathogenetic and therapeutic considerations
The PreS2 activator MHBs(t) of hepatitis B virus activates c-raf-1/Erk2 signaling in transgenic mice
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Apoptosis
Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis