Dissection of experimental asthma with DNA microarray analysis identifies arginase in asthma pathogenesis
J. Clin. Invest. Nives Zimmermann, et al. 111:1863 doi:10.1172/JCI17912 [
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Figure 3Northern blot and arginase activity analysis. In
a, Northern blot analysis of arginase I and arginase II expression after OVA challenge is shown. Time points are as follows: 3H = 1 challenge, 3 hours; 18H = 1 challenge, 18 hours; 2C = 2 challenges, 18 hours. The EtBr–stained gel is also shown. The autoradiograph exposure times were 18 hours and 2 days for arginase I and arginase II, respectively. In
b, the expression of arginase I and arginase II after intranasal challenges with
A. fumigatus or saline is shown. Sal, saline; Asp, aspergillus. The autoradiograph exposure times were 18 hours and 6 days for arginase I and arginase II, respectively. In
a and
b, each lane represents a separate mouse. In
c, arginase activity in the lungs of saline- and OVA-challenged mice (
n = 4 mice and
n = 3 mice, respectively) is shown. Arginase activity was measured in lung lysates with the use of the blood urea nitrogen reagent. As a control, arginase activity in the liver was 1522 ± 183 and 1390 ± 78 nmol/min/mg protein for saline- and OVA-challenged mice, respectively. In
d, putrescine levels in the whole lungs of saline- and OVA-challenged mice (
n = 4 mice and
n = 7 mice, respectively) are shown. Putrescine levels were determined by HPLC.
