Mesenchymal stem cell implantation in a swine myocardial infarct model: engraftment and functional effects Jay G. Shake, MD, Peter J. Gruber, MD, PhD,

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Presentation transcript:

Mesenchymal stem cell implantation in a swine myocardial infarct model: engraftment and functional effects Jay G. Shake, MD, Peter J. Gruber, MD, PhD, William A. Baumgartner, MD, Guylaine Senechal, MS, Jennifer Meyers, BS, J.Mark Redmond, MD, Mark F. Pittenger, PhD, Bradley J. Martin, PhD The Annals of Thoracic Surgery Volume 73, Issue 6, Pages 1919-1926 (June 2002) DOI: 10.1016/S0003-4975(02)03517-8

Fig 1 Location of the left ventricle infarct (A) and spatial orientation of the piezoelectric crystals (B). An endocardial and epicardial pair of crystals measured the wall thickness and active wall thickening during the cardiac cycle. Two mid-myocardial crystals measured the segment shortening. Mesenchymal stem cells were directly injected in the localized region between the piezoelectric crystals. The Annals of Thoracic Surgery 2002 73, 1919-1926DOI: (10.1016/S0003-4975(02)03517-8)

Fig 2 End diastolic wall thickness as measured by sonomicrometry. Note the extent of left ventricular wall thinning in the control group after production of the left ventricular infarct. Mesenchymal stem cell (MSC) implantation resulted in an attenuation of wall thinning when compared with control animals at all time points. Data are group averages and presented as mean ± SEM. The Annals of Thoracic Surgery 2002 73, 1919-1926DOI: (10.1016/S0003-4975(02)03517-8)

Fig 3 Systolic wall thickening as measured via sonomicrometry and expressed as a percent of baseline values. Myocardial infarction resulted in a marked reduction in contractile function in both control and treated animals. While paradoxic wall thinning was observed in control animals (negative thickening values), mesenchymal stem cell (MSC) implantation significantly reduced the degree of systolic dysfunction. Differences between the two groups were evident by 2 weeks and became statistically significant by 4 weeks. Data are group averages and presented as mean ± SEM. ∗p < 0.05 versus control. The Annals of Thoracic Surgery 2002 73, 1919-1926DOI: (10.1016/S0003-4975(02)03517-8)

Fig 4 Gross left ventricular (LV) cross-sections at the level of mesenchymal stem cell (MSC) injection and piezoelectric crystal placement. Large transmural infarctions were observed in all animals. Control animals (top row) had wall thinning and loss of normal ventricle chamber geometry associated with remodeled infarctions. MSC-treated animals (bottom row) had preserved wall thickness and LV geometry. (IFN = interferon.) The Annals of Thoracic Surgery 2002 73, 1919-1926DOI: (10.1016/S0003-4975(02)03517-8)

Fig 5 Mesenchymal stem cell (MSC) engraftment and muscle-specific protein-expression using immunohistochemistry. The Di-I labeled mesenchymal stem cells (red) and muscle protein-specific antibodies (green) fluoresce under confocal microscopy. Colocalization (yellow) confirms cells having both probes present. Specifically this represents specific muscle protein expression within the MSCs being imaged. (B) This hematoxylin and eosin (H&E)–stained serial section corresponds to (A) illustrating a cluster of MSC in proximity to host myocardium. Several muscle-specific proteins were identified in treated myocardium. Examples include α-actinin (α-act) (A and D), troponin T (TnT) (C), phospholamban (PLB) (E), and tropomyosin (TM) (F) expression at 4 weeks postimplantation. The Annals of Thoracic Surgery 2002 73, 1919-1926DOI: (10.1016/S0003-4975(02)03517-8)