Inhibition of endogenous thioredoxin in the heart increases oxidative stress and cardiac hypertrophy
J. Clin. Invest. Mitsutaka Yamamoto, et al. 112:1395 doi:10.1172/JCI17700 [Go to this article.]

Figure 1
(a) Heart homogenates were prepared from Tg-DN-Trx1 and NTg mice. Immunoblot analyses were conducted using anti-hTrx1 Ab. Short (15-second) and long (5-minute) exposures of the immunoblot are shown. After long exposure, endogenous mouse Trx1 was detected. Note that the anti-hTrx1 Ab (clone 2G11) does not detect mouse Trx1 as efficiently as it detects hTrx1. (b) Tissue homogenates were prepared from various organs. Immunoblot analyses were conducted using anti-hTrx1 Ab. (c) RT-PCR analyses of Trx1 and GAPDH. Total RNA was extracted from Tg-DN-Trx1 (line no. 13) and NTg mice. The lower left panel indicates protein expression of total Trx1, determined using anti-hTrx1 Ab (clone 4H9), which detects both mouse Trx1 and hTrx1. (d) The disulfide oxidoreductase activity of Trx was determined by the insulin reduction assay. Time-dependent reduction of NADPH, determined by spectrophotometry, is shown. *P < 0.01 compared with NTg. ^#P < 0.05, ^##P < 0.01 compared with 0 min.