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1 Department of Medicine, Shiga University of Medical Science, Shiga 520-2192; and 2 Discovery Research Laboratory, Tanabe Seiyaku Company, Limited, Osaka, Japan
Persistent proteinuria has been indicated
to be a major risk factor for the development of tubulointerstitial
damage through a process of proinflammatory molecule expression.
Monocyte chemoattractant protein-1 (MCP-1) was shown to contribute to
recruitment of immune cells into the renal interstitium in acute and
chronic renal diseases. However, the molecular mechanisms by which
proteinuria causes MCP-1 expression in proximal tubular cells have not
been fully clarified. In this study, we examined whether albumin
overload-induced MCP-1 expression was regulated by mitogen-activated
protein kinase (MAPK) in mouse proximal tubular (mProx) cells. Exposure
of mProx cells to delipidated bovine serum albumin (BSA) induced mRNA
and protein expression of MCP-1 in a time- and dose-dependent manner. BSA activated extracellular signal-regulated kinase (ERK1/2) and p38
MAPK. The MEK inhibitor U-0126 partially suppressed BSA-induced MCP-1
expression and MCP-1 promoter/luciferase reporter activity. U-0126 also
inhibited an increase in nuclear factor-
B and activator protein-1
DNA-binding activity of MCP-1 promoter by protein overload in mProx
cells. In addition, we found that U-0126 inhibited BSA-induced nuclear
factor-B reporter activity and inhibitory protein degradation in
mProx cells. In conclusion, these findings indicate that ERK signaling
is involved in BSA-induced MCP-1 expression in mProx cells.
nuclear factor-B; tubulointerstitial damage
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