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. 2019 Jul 31;8(15):e012047. doi: 10.1161/JAHA.119.012047

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© 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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MURC (muscle‐restricted coiled‐coil protein) deficiency ameliorates reactive oxygen species (ROS) production in the heart after ischemia/reperfusion (I/R). A and B, Cardiac ROS production as measured by dihydroethidium staining of left ventricle tissue from mouse hearts with confocal micrographs and Z‐stack–generated 2.5‐dimensional reconstructions. Representative dihydroethidium staining (A) and quantification (B) of wild‐type (WT) and MURC knockout (MURC KO) mouse hearts after sham operation or 30 minutes after I/R. Scale bar=100 μm. C through F, Measurement of mRNA expressions (C and E) and the protein levels (D and F) of EGR1 (early growth response protein 1) and DDIT4 (DNA‐damage‐inducible transcript 4) in WT and MURC KO mouse hearts after sham operation or 24 hours after I/R; n=5 per group. *P<0.05, **P<0.01. Data are presented as mean±SEM.