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Additional Supporting Information may be found in the online version of this article.

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STEM_789_sm_suppFigure1.pdf1082KFigure S1. Experimental Protocol. (A). In vitro protocol, arrows indicate time points for treatment, performance of simulated ischemia/reoxygenation, and measurement of various parameters for each experimental group. (B). In vivo protocol. Arrowheads indicate sites of injection of adipose-derived stem cells in the border zone of the infarcted heart.
STEM_789_sm_suppFigure2.pdf957KFigure S2. Effect of PDE-5 inhibition on protection of ASCs. Quantitative data showing the effect of sildenafil (SIL) or shRNAPDE-5 on necrosis following SI-RO as determined by MTS cell viability assay (A) and LDH release (B). (C) Representative images of TUNEL assay (10 x magnification). (* indicates p<0.01 versus SI-RO, shCON ASC; n=8).
STEM_789_sm_suppFigure3.pdf955KFigure S3. Sildenafil protects ASCs against ischemia/reoxygenation injury through PKG. Quantitative data showing the effect of KT 5823 (KT) and shRNAPKG on necrosis following SIRO as determined by MTS cell viability assay (A) and LDH release (B). (C) Representative images of TUNEL assay (10 x magnification). (* indicates p<0.01 versus SI-RO, shCON ASC; n=8).
STEM_789_sm_suppFigure4.pdf1183KFigure S4. Transplantation of preconditioned ASCs improves cardiac function and remodeling following myocardial infarction. (A) Representative M-mode images showing preservation of LV contractility of hearts treated with preconditioned ASCs as compared with non-treated ASCs control following myocardial infarction (MI). (B). Bar diagram showing quantitative data of LV fractional shortening.

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