FIGURE 3
FROM:
PAI-1 deficiency attenuates the fibrogenic response to ureteral obstruction
Takashi Oda, Young Ok Jung, Heung Soo Kim, Xiaohe Cai, Jesús M López-Guisa, Yukiko Ikeda and Allison A Eddy
BACK TO ARTICLEFigure 3.
(A) Representative Northern blot autoradiograph of renal mRNA levels for plasminogen-activator inhibitor-1 (PAI-1), tissue-type plasminogen activator (tPA), urokinase-type plasminogen activator (uPA), and 
2-antiplasmin (2-AP). The graph shows the results of PAI-1 Northern blotting when RNA from each experimental animal was loaded into separate wells, expressed in arbitrary units as mean 
1 SD (B). No PAI-1 mRNA band was detected in the kidneys of the -/- mice. *P < 0.05 compared with sham controls of the same genotype. Similar analyses (data not shown) found a significant 50% increase in uPA only at 7D after UUO and a 300 to 400% increase in tPA at 3D, 7D, and 14D after UUO compared with sham kidneys, and a significant 20 to 60% decrease in 
2-AP at all time points. There were no differences in the tPA, uPA, and 2-AP responses between the +/+ and -/- mice.
