Hong-Zhu Lu1, Jian-Hua Zhou. 1. Deptartment of Pediatrics, Clinical Medical College, Yangtze University, Jingzhou 434000, China.
Abstract
OBJECTIVE: To investigate the effects of hepatitis B virus (HBV) X protein (HBx) on the expression of tumor necrosis factor-α (TNF-α) in glomerular mesangial cells (GMCs) and the underlying intracellular signal pathways. METHODS: The plasmid pCI-neo-X that carries the X gene of hepatitis B virus was transfected into cultured GMCs. HBx expression in the transfected GMCs was assessed by Western-blot. TNF-α protein and mRNA were assessed by ELISA and semi-quantitative RT-PCR, respectively. Three kinase inhibitors-U0126, an inhibitor of extracellular signal-regulated kinases (ERKs); lactacystin, an inhibitor of nuclear factor-κB (NF-κB); and SB203580, a selective inhibitor of p38 MAP kinase (p38 MAPK) were used to determine which intracellular signal pathways may underlie the action of HBx on TNF-α expression in transfected GMCs. RESULTS: A significant increase in HBx expression in pCI-neo-X transfected GMCs was detected at 36 h and 48 h, which was not affected by any of those kinase inhibitors mentioned above. A similar increase in the expression of both TNF-α protein and mRNA was also observed at 36 h and 48 h, which was significantly decreased in the presence of U0126 or lactacytin, but not SB203580. CONCLUSIONS: HBx upregulates TNF-α expression in cultured GMCs, possibly through ERKs and NF-κB pathway, but not p38 MAPK pathway.
OBJECTIVE: To investigate the effects of hepatitis B virus (HBV) X protein (HBx) on the expression of tumor necrosis factor-α (TNF-α) in glomerular mesangial cells (GMCs) and the underlying intracellular signal pathways. METHODS: The plasmid pCI-neo-X that carries the X gene of hepatitis B virus was transfected into cultured GMCs. HBx expression in the transfected GMCs was assessed by Western-blot. TNF-α protein and mRNA were assessed by ELISA and semi-quantitative RT-PCR, respectively. Three kinase inhibitors-U0126, an inhibitor of extracellular signal-regulated kinases (ERKs); lactacystin, an inhibitor of nuclear factor-κB (NF-κB); and SB203580, a selective inhibitor of p38 MAP kinase (p38 MAPK) were used to determine which intracellular signal pathways may underlie the action of HBx on TNF-α expression in transfected GMCs. RESULTS: A significant increase in HBx expression in pCI-neo-X transfected GMCs was detected at 36 h and 48 h, which was not affected by any of those kinase inhibitors mentioned above. A similar increase in the expression of both TNF-α protein and mRNA was also observed at 36 h and 48 h, which was significantly decreased in the presence of U0126 or lactacytin, but not SB203580. CONCLUSIONS:HBx upregulates TNF-α expression in cultured GMCs, possibly through ERKs and NF-κB pathway, but not p38 MAPK pathway.
Entities:
Keywords:
Extracellular signal-regulated kinase; Glomerulonephritis; Heptitis B virus; Nuclear factor-κB; Tumor necrosis factor-α; X protein
Authors: Laurinda A Cooker; Darryl Peterson; Joann Rambow; Melisa L Riser; Rebecca E Riser; Feridoon Najmabadi; David Brigstock; Bruce L Riser Journal: Am J Physiol Renal Physiol Date: 2007-03-20
Authors: Joseph C K Leung; Sydney C W Tang; Loretta Y Y Chan; Wai Long Chan; Kar Neng Lai Journal: Nephrol Dial Transplant Date: 2007-09-26 Impact factor: 5.992