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1 Department of Medicine, Shiga University of Medical Science, Otsu, Shiga, Japan
2 Discovery Research Laboratory, Tanabe Seiyaku Co., Ltd.,, Osaka, Osaka, Japan
* To whom correspondence should be addressed. E-mail: haneda{at}belle.shiga-med.ac.jp.
Persistent proteinuria has been indicated to be a major risk factor for the development of tubulointerstitial damage through a process as proinflammatry molecules expression. Among these, monocyte chemoattractant protein-1 (MCP-1) was shown to contribute to the recruitment of immune cells into the renal interstitium in both 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 yet.
In this study, we examined whether albumin overload-induced MCP-1 expression was regulated by MAPK family in mouse proximal tubular cells (mProx). By exposing mProx to delipidated bovine serum albumin (BSA), mRNA and protein expression of MCP-1 was induced in a time-and dose-dependent manner. BSA was able to activate extracellular signal-regulated kinases 1/2 (ERK1/2) and p38 MAPK. MEK inhibitor (U0126) partially suppressed BSA-induced MCP-1 expression and MCP-1 promoter / luciferase reporter activity. U0126 also inhibited an increase in NF-
B and AP-1 DNA binding activity of MCP-1 promoter by protein overload in mProx. In addition, we found that U0126 inhibited BSA-induced NF-B reporter activity and IB-
degradation in mProx.In conclusion, these findings indicate that ERK signaling is involved in BSA induced MCP-1 expression in mProx.
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