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. 2019 Oct 25;8(21):e012575. doi: 10.1161/JAHA.119.012575

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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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TRAF1 deficiency decreased I/R‐induced apoptosis. A, Immunofluorescence staining and positive cell‐count results of TUNEL in heart tissues (n=3 per group). Blue indicates nuclei; green indicates TUNEL positive staining. B, Relative mRNA levels of apoptosis‐related molecules in heart tissues (n=4 per group). C, Western blot and quantitative results of apoptosis‐related protein expression levels in sham and I/R groups. Results shown are representative of 3 blots, GAPDH served as loading control. For statistical analysis, a 2‐tailed Student t test was used for panels B and C. **P<0.01. Bax indicates BCL2 associated X, apoptosis regulator; Bcl2, BCL2 apoptosis regulator; C‐Casp3, cleaved caspase 3; HPF, high‐power filed; I/R, ischemia/reperfusion; KO, knockout; TRAF1, tumor necrosis factor receptor–associated factor 1; TUNEL, terminal deoxynucleotidyl transferase dUTP nick‐end labeling; WT, wild type.