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. Author manuscript; available in PMC: 2016 Apr 21.
Published in final edited form as: JCI Insight. 2016;1(2):e85817. doi: 10.1172/jci.insight.85817

Figure 2. Heme oxygenase-1 overexpression protects cardiomyocytes from doxorubicin-mediated damage.

Figure 2

(A and B) Representative micrographs of midsagittal sections of cardiac left ventricle (LV) from WT and humanized heme oxygenase-1 (HO-1) overexpressing (HBAC) mice 14 days after doxorubicin (DOX) treatment. Cross sections stained with H&E from (A) WT or (B) HBAC mice. Scale bar: 1 mm. (C–F) H&E-stained sections demonstrating that HO-1 overexpression prevents cardiomyocyte vacuolization (black arrows), hypereosinophilia (red arrows), and interstitial edema (asterisks) observed in WT mice. Scale bar: 100 μm. (G and H) Trichrome staining for fibrosis in the LV of WT and HBAC mice. Scale bar: 100 μm. Slides were assessed by a pathologist blinded to the different groups. n = 3–6 per group. (I) Mononuclear phagocyte (CD45+CD11b+Gr-1−MHCII+) infiltration into the LV of WT and HBAC mice treated with DOX or vehicle was quantified by flow cytometry and expressed as a proportion of CD45+ cells. Horizontal bars represent mean values. *P < 0.05, **P < 0.01, ANOVA and the Newman-Keuls post-test were used to determine statistically significant changes; n = 3–5 per group.