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Protein alteration of H ep G 2.2.15 cells induced by iron overload
Author(s) -
Fang Caiyun,
Zhao Chao,
Liu Xiaohui,
Yang Pengyuan,
Lu Haojie
Publication year - 2012
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.201100335
Subject(s) - hepatitis b virus , signal transduction , apoptosis , secretion , chemistry , microbiology and biotechnology , stimulation , antigen , biology , biochemistry , virus , immunology , endocrinology
Hepatitis B can progress into hepatocellular carcinoma. Body irons may interfere with the clearance of hepatitis B virus ( HBV ) and contribute to genesis of tumor. To investigate the role of iron played in HBV ‐related pathogenesis, here we studied the effect of iron with different concentrations and valence states on growth of H ep G 2.2.15 cells and secretion of virus proteins. A strong tolerance of H ep G 2.2.15 cells to iron challenge was found. The concentration of hepatitis B surface antigen in cell culture medium was decreased after iron stimulation. Lower concentrations of iron facilitated hepatitis B e‐antigen ( HB e A g) secretion. F e 2+ appeared more effective on HB e A g secretion than F e 3+ did. In parallel, the differential protein profiles in H ep G 2.2.15 cells were studied by i TRAQ and LC ‐ MS / MS . The differentially expressed proteins were mainly involved in stress response, signal transduction, apoptosis, etc. Four proteins (14‐3‐3 β/α, VCP , migration inhibitory factor, and N up153) were verified by Western‐blotting and found to be consistent with the i TRAQ data. Interestingly, nuclear import of Nuclear factor kappa B ( NF κ B ) and its activity were found to be affected by the decreased N up153 in iron stimulated H ep G 2.2.15 cells. The results may indicate possible molecular mechanism how the synergism of HBV and iron stimulation damages host liver cells.