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. 2013 Feb 13;304(8):F1054–F1065. doi: 10.1152/ajprenal.00650.2012

Fig. 1.

Fig. 1.

Netrin-1 overexpression in proximal tubular epithelial cells accelerates recovery of kidney function in response to ischemia-reperfusion (IR) injury. A: a wild-type (WT) kidney does not show any staining for transgene chicken netrin-1. B: transgenic mouse kidney showing staining for chicken netrin-1 in proximal tubular epithelial cells. Some proximal tubules are not stained for chicken netrin-1. The reason for this is unclear. C: serum creatinine was measured at various time points after reperfusion in WT and netrin-1 transgenic mice subjected to sham operation or ischemia followed by reperfusion (IR). Values are means ± SE. *P < 0.01 vs. WT IR; n = 6 for each group. D: proximal tubular injury marker KIM-1 excretion was determined by ELISA at 2 wk after reperfusion. Kidney injury molecule-1 (KIM-1) excretion is increased after IR in WT mice, which was suppressed in netrin-1 transgenic animal subjected to IR. *P < 0.001 vs. sham. #P < 0.001 vs. WT IR; n = 6.