BACKGROUND: Netrin-1 is a laminin-related secreted protein, is highly induced 
after tissue injury, and may serve as a marker of injury. However, the 
regulation of netrin-1 production is not unknown. Current study was carried out 
in mouse and mouse kidney cell line (TKPTS) to determine the signaling pathways 
that regulate netrin-1 production in response to injury.
METHODS AND PRINCIPAL FINDINGS: Ischemia reperfusion injury of the kidney was 
induced in mice by clamping renal pedicle for 30 minutes. Cellular stress was 
induced in mouse proximal tubular epithelial cell line by treating with 
pervanadate, cisplatin, lipopolysaccharide, glucose or hypoxia followed by 
reoxygenation. Netrin-1 expression was quantified by real time RT-PCR and 
protein production was quantified using an ELISA kit. Cellular stress induced a 
large increase in netrin-1 production without increase in transcription of 
netrin-1 gene. Mitogen activated protein kinase, ERK mediates the drug induced 
netrin-1 mRNA translation increase without altering mRNA stability.
CONCLUSION: Our results suggest that netrin-1 expression is suppressed at the 
translational level and MAPK activation leads to rapid translation of netrin-1 
mRNA in the kidney tubular epithelial cells.