Fig. 1.

Human MiPs display differential myogenic propensity in vivo. a Validation of NIS transgene functionality for PET imaging by quantitation of ^99mTcO₄ ⁻ uptake in vitro. *Kruskal–Wallis test and Mann–Whitney U-test vs ctrl, P < 0.05, n = 3/cohort. Scale bar ∼100 µm. b Validation of iCasp9 transgene by viable cell count after AP20187 administration in vitro. Only iCasp9+MiPs did significantly undergo progressive cell death, which appeared virtually complete after 48 h. *Two-way ANOVA with Bonferroni correction, P < 0.05 (interaction), n = 3/cohort. Data points depict average and min-to-max span for each sample. c 1 week after injection, PET scan of live animals shows engraftment of GIN+MiPs in heart (H) and hindlimbs (HL) muscles of only MiP-treated mice. T, thymus, S, stomach, B, bladder; endogenous positive PET signals. d SUV levels in heart and hindlimb regions of PET-scanned mice. *P < 0.05 vs sham; **P < 0.05 vs sham and fibroblast-MiPs; Kruskal–Wallis and Mann–Whitney U test; n = 3/cohort. e Stereofluorescence analysis of heart and hindlimb (gastrocnemius) muscles of recipient mice before (4 weeks p.i.) and after (8 weeks p.i.) AP20187 administration. f Live fluorescence and cytometry analyses of CD56-isolated SCs and AP-isolated MABs from recipient mice at end-point.both SCs and Mabs MAB-MiP-treated animals displayed larger GFP⁺ subfractions than fibroblast-MiP-treated ones and GFP⁺ cells were undetectable after AP20187 administration **P < 0.05 vs fibroblast-MiP-treated mice; Kruskal–Wallis and Mann–Whitney U test; n = 3/cohort at end-point, scale bar ∼100 µm