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. 2016 Mar 17;118(6):970–983. doi: 10.1161/CIRCRESAHA.115.307516

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© 2016 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDervis License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 5. — Hypoxia-preconditioned bone marrow mesenchymal stem cells (HP-MSCs) transplantation promotes cardiomyocyte proliferation and angiogenesis after myocardial infarction (MI). A–D, Proliferating cells were identified on day 28 after MI and treatment by staining for expression of the proliferation marker Ki67 (red) in (A) sections of noninfarcted tissue from the right ventricle (RV) of animals in the HP-MSCs group and in sections from the border zone of the infarct in hearts from animals in the Dulbecco’s Modified Eagle’s Medium (DMEM; B), normal cultured bone marrow mesenchymal stem cells (N-MSCs; C), and HP-MSCs groups (D). Cardiac tissue was visualized via fluorescent immunostaining for TnI (green), and nuclei were counterstained with Hoechst 33258 (bar=100 μm); the boxed regions of merged images are also displayed at higher magnification (yellow bar=50 μm). E, Proliferation was quantified as the number of Ki67⁺cells per high-power field (HPF), and (F) cardiomyocyte proliferation was quantified as the number of cells that expressed both Ki67and TnI per HPF. G–J, Endothelial cells were identified on day 28 after MI and treatment by staining for expression of the endothelial marker CD31 (red) in (G) sections of noninfarcted tissue from the right ventricle (RV) of animals in the HP-MSCs group and in sections from the border zone of the infarct in hearts from animals in the DMEM (H), N-MSCs (I), and HP-MSCs groups (J); nuclei were counterstained with Hoechst 33258 (bar=100 μm). K–N, Smooth muscle cells were identified on day 28 after MI and treatment by staining for expression of smooth muscle actin (SMA; red) in (K) sections of noninfarcted tissue from the right ventricle (RV) of animals in the HP-MSCs group and in sections from the border zone of the infarct in hearts from animals in the DMEM (L), N-MSCs (M), and HP-MSCs groups (N); nuclei were counterstained with Hoechst 33258 (bar=100 μm). Vascular density was quantified as the number of CD31⁺cells per HPF (O), and arteriole density was quantified as the number of SMA⁺ cells per HPF (P).