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ia ra ef luciferase (Fluc) and the human sodium iodide transporter (hNIS) to allow cell monitoring via bioluminescence imaging (BLI) and- rectly labeled via incorporation of imaging reporter genes in the DNA of the cell and the encoded protein will specif-MABs in vivo is currently available. This allows cellmonitoring via clinically establishednonin-emissionstem cell engraftment in preclinical research. However, this is an invasive technique, which provides no whole tomography (PET) and single-photon emission computed tomography (SPECT) (Chung, 2002).To date, histology is the gold standard for evaluating vasive imaging approaches, namely positronbrane fragility and contraction-mediated muscle injury. At present, no regenerative therapy for MDs is available and glucocorticoids are the only clinically accepted, disease-delaying drugs with serious long-term side effects (Bushby et al., 2010). In healthy individuals, damaged muscles are restored by endogenous stem cells. This natural process of repair formed the basis of evaluating different stem cells for their regenerative potential in MDs. Our group has demon-strated that mesoangioblasts (MABs), which are vessel-derived stem cells, have therapeutic potential in several preclinical models of MDs (Sampaolesi et al., 2003, 2006). These positive results have led to a phase 1 clinical study in Duchenne (D)MD patients with HLA-matched MABs (EudraCT #2011-000176-33) (Cossu et al., 2015). Despite progress into clinical trial, limited information about the biodistribution and long-term survival of ically convert a substrate or bind and/or take up a reporter probe. This has some major advantages compared to direct labeling, as it allows long-term cell monitoring and reflects cell viability. Both factors are of crucial importance to eval-uate and optimize stem cell therapy. To visualize graft survival in vivo, mMABs were trans-duced with a lentiviral vector encoding a bicistronic imag-ing reporter gene construct encoding firefly luciferas