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. 2015 Jul 21;4(7):e002153. doi: 10.1161/JAHA.115.002153

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© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Reduction of cardiac Txnrd2 expression by tamoxifen administration. A, Generation of Txnrd2^{−/fl;Tg[MerCreMer]} (knockout, ko) and Txnrd2^{+/fl;Tg[MerCreMer]} (control, ctrl) mice. B, To inactivate Txnrd2, 6-week-old ko and ctrl mice were treated with tamoxifen for 5 weeks. The end of tamoxifen treatment was defined as week 0. C, Semiquantitative RT-PCR 4 weeks after feeding tamoxifen-containing diet confirmed reduction of Txnrd2mRNA. D, Reduced Txnrd2mRNA shown by RT-PCR of whole heart cDNA. mRNA expression was normalized to Gapdh. Each column represents 3 independent cDNA samples (n=3). E, Reduced TXNRD2 expression in Western blot of cytosolic and mitochondrial protein fractions from whole hearts. ACTIN served as cytosolic and VDAC1 as mitochondrial loading control. αMHC indicates alpha-myosin heavy chain; RT-PCR, real-time polymerase chain reaction; TXNRD2, thioredoxin reductase 2; VDAC1, voltage-dependent anion-selective channel protein 1.