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KMID : 1161520160200060317
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Animal Cells and Systems
2016 Volume.20 No. 6 p.317 ~ p.324
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Zinc induces LPS-mediated upregulation of HBD-2 via ERK1/2 and p38MAPK signaling pathways in human prostate epithelial cells
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Kim Min-Su
Ko Ki-Sung
Kim Hae-Jong
Lee Jae-Hyouk
Myung Soon-Chul
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Abstract
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This study aimed to clarify the role of zinc in human prostate epithelial cell defense against bacterial infection. To explore the effect of zinc on lipopolysaccharide (LPS)-mediated induction of human β-defensin-2 (HBD-2), the normal human prostate epithelial cell lines (RWPE-1) were co-treated with zinc/LPS and HBD-2 mRNA expression was quantitated by the reverse transcription polymerase chain reaction (RT-PCR). We also conducted a Western blot analysis to determine whether zinc stimulates p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase-1 and -2 (ERK1/2) signaling pathways. To investigate the involvement of the p38MAPK and ERK1/2 signaling pathways in zinc-mediated upregulation of HBD-2, quantitative real-time PCR and immunocytochemical staining were then used to quantify HBD-2 mRNA expression and protein production, respectively, which was treated with either U0126 (ERK1/2 inhibitor) or SB203580 (p38MAPK inhibitor) prior to each analysis of HBD-2. Cotreatment of RWPE-1 cells with zinc/LPS-upregulated HBD-2 expression to an even greater extent than either LPS alone or zinc alone. Moreover, the treatment of RWPE-1 cells with zinc significantly increased both the total and phosphorylated forms of ERK1/2 and p38MAPK. ERK1/2 and p38MAPK signaling via the inhibitors U0126 and SB203580 pharmacologically inhibited zinc-mediated upregulation of HBD-2. These results strongly suggest that zinc plays an important role in the immune response of the prostate. Furthermore, we demonstrate that zinc-mediated upregulation of HBD-2 expression upon bacterial infection of prostate epithelial cells involves the ERK1/2 and p38MAPK signaling pathways.
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KEYWORD
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Prostate, zinc, HBD-2, LPS, MAPK
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