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. Author manuscript; available in PMC: 2015 Mar 19.
Published in final edited form as: Sci Transl Med. 2013 Oct 16;5(207):207ra141. doi: 10.1126/scitranslmed.3006479

Fig. 5. Deletion of Tnni3k reduces infarct size, cardiomyocyte loss, and p38 MAPK activation after I/R.

Fig. 5

(A) TNNI3K protein levels in the LV of inducible cardiomyocyte-specific Tnni3k-KO mice or Tnni3k-floxed (fl/fl), Mer-Cre-Mer–negative (MCM−/−) WT littermate controls, 5 days after the final dose of tamoxifen. (B) Representative Evans blue– and triphenyltetrazolium chloride (TTC)–stained LV sections from Tnni3k-KO mice or WT controls (n = 11 per group). (C) Infarct sizes as a percentage of the AAR. (D) AAR per total LV. (E) Plasma levels of cTnI, plasma troponin T (cTnT), and myosin light chain (MLC). (F) Representative continuous immunoblots (n = 6 animals per group) for phosphorylation status of Akt, ERK1/2, JNK1/2, or p38 MAPK in the remote LV of Tnni3k-KO or WT mice. TNNI3K and GAPDH are shown as controls. Quantification is shown on the right. All measurements in (B) to (F) were made 24 hours after I/R. All data in (C) to (F) are means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, two-tailed Student’s t test.