Cardiac CEST-MRI for tracking stem cell survival and determining the role of CXCL2

Background Because of the limited endogenous repair mechanisms that exist in the heart, exogenous stem cell therapies offer the potential to provide the building blocks for repair and/or evoke developmental pathways to recruit endogenous cells that can prevent adverse remodeling and promote healing. MR-labeling of stem cells with iron oxides has been used to track stem cells in the heart, but cannot distinguish viable stem cells from cells that have died and released iron oxides. In contradistinction, reporter gene labeling offers the advantage that the reporter is only produced by viable cells. Recently, chemical exchange saturation transfer (CEST) MRI has been performed in the heart (cardioCEST) to endogenously detect fibrosis after myocardial infarction in mice (Vandsburger, M. et al. Circ Cardiovasc Imaging 8, (2015)). In this study, we seek to image reporter genelabeled mesenchymal stem cells (MSCs) in an in vivo pig model using cardioCEST MRI.