Volume 23, Issue 2, Pages 95-104 (June 2016) Experimental induction of reparative morphogenesis and adaptive reserves in the ischemic myocardium using multipotent mesenchymal bone marrow-derived stem cells  V.Yu. Mykhaylichenko, A.V. Kubyshkin, S.A. Samarin, I.I. Fomochkina, L.V. Anisimova  Pathophysiology  Volume 23, Issue 2, Pages 95-104 (June 2016) DOI: 10.1016/j.pathophys.2016.04.002 Copyright © 2016 Elsevier B.V. Terms and Conditions

Fig. 1 Echocardiographic parameters of heart functioning in rats: LVIDd—end-diastolic left ventricular internal dimensions; LVIDs—end-systolic left ventricular internal dimensions; FS—fractional shortening, EF—ejection fraction. Group a − rats with MI without post-MI treatment; Group b − rats with MI+transplantation of MSC; Group c − rats MI+transplantation of committed MSC. Statistical significance was determined using a two-tailed paired Student’s t-test (р<0.05). * compared with the control; ** compared with the group of rats with MI without therapy. Pathophysiology 2016 23, 95-104DOI: (10.1016/j.pathophys.2016.04.002) Copyright © 2016 Elsevier B.V. Terms and Conditions

Fig. 2 Histological sections of areas with ischemic infarction. A-B Experimental models (rats) with myocardial infarction without post-MI treatment, showing coagulative necrosis (3rd day after MI modelling) and a large scar at the site of the transmural MI, and formation of an aneurysm (30th day after MI modelling). C Experimental models (rats) with MI+transplantation of committed MSC, showing the alternation of muscle areas that have survived, and the field of scar tissue, as well as the absence of aneurysm (30th day after MI modelling). Staining with hematoxylin and eosin, ×10 (A, C); ×30 (B). Pathophysiology 2016 23, 95-104DOI: (10.1016/j.pathophys.2016.04.002) Copyright © 2016 Elsevier B.V. Terms and Conditions

Fig. 3 The morphometric investigation showing quantative analysis. A Vascular morphometry with myocardial infarction and formation of scar tissue. B The morphometry of the connective tissue and myocardial infarction. Pathophysiology 2016 23, 95-104DOI: (10.1016/j.pathophys.2016.04.002) Copyright © 2016 Elsevier B.V. Terms and Conditions

Fig. 4 The immunohistochemical sections identifying actin, troponin, and proliferating cells. A-B Experimental model (rat) with myocardial infarction without treatment. A large single scar is observed that retains beams of muscle fibers in the subepicardial sections accompanied by the presence of proliferated connective tissue cells. С-D Experimental model (rat) with myocardial infarction+transplantation of committed MSC, showing alternation of beams of saved cardiomyocytes and scar tissue. Immunohistochemical stain with primary antibodies to troponin T, ×30 (A, C); immunohistochemical stain with primary antibodies to actin, ×150 (B, D). Pathophysiology 2016 23, 95-104DOI: (10.1016/j.pathophys.2016.04.002) Copyright © 2016 Elsevier B.V. Terms and Conditions

Fig. 5 Immunohistochemical analysis and data from in situ hybridization. A–D Experimental models (rats) with myocardial infarction without treatment. Cells in the rumen and the vessel walls do not contain the Y chromosome. B–E Experimental models (rats) with myocardial infarction and transplantation of MSC. Positive staining of vascular wall cells, connective tissue, and immediate surroundings for the Y chromosome post transplantation of MSC. С–F Experimental models (rats) with myocardial infarction and transplantation of committed MSC. Positive staining of cells containing the Y chromosome in the connective tissue of female rats on the 30th day after transplantation with cMSC. In situ hybridization with a marker for the Y chromosome, ×150 (A, C, D); ×180 (B); ×300 (E, F). G Positive control (chromosome 12) in the myocardium of rats after transplantation with cMSC (30the day). In situ hybridization with a marker to chromosome 12, ×150. Pathophysiology 2016 23, 95-104DOI: (10.1016/j.pathophys.2016.04.002) Copyright © 2016 Elsevier B.V. Terms and Conditions