Fig. 6: H2 clone transplanted into mouse immunocompromised dystrophic model is more resistant and have a higher integration capability | Cell Death & Disease

Fig. 6: H2 clone transplanted into mouse immunocompromised dystrophic model is more resistant and have a higher integration capability

From: Oxidative stress preconditioning of mouse perivascular myogenic progenitors selects a subpopulation of cells with a distinct survival advantage in vitro and in vivo

Fig. 6

a LacZ qRT-PCR of A6 cells and cell clone. RNA was isolated from the treated TA 48 h after mabs intramuscular injection. b Immunohistochemistry against laminin (brown) and X-Gal staining (blue) on TA section showing A6 cells a-c and H2 cell clone d-f, modified for nLacZ and implanted intramuscularly in mouse dystrophic model, after 20 days from injection. Dotted boxes in a and d indicate areas of enlarged view (b, e) revealing LacZ positive nuclei into host TA, showing in e integrated LacZ positive nuclei inside regenerating host myofibers. The images in a and d are collage resulting to obtain whole TA section images. a, d Magnification 10X, b, e magnification 20X, c, f magnification 40X. Scale bars: a 300 μm; b) 40 μm; c 20 μm. c Number of LacZ positive nuclei of A6 cells and cell clone injected in the muscle. The data are representative from three independently experiments. The error bars indicate standard deviation. **P < 0.05, ***P < 0.005. d Muscle recovery upon 40 days H2 treatment. a-d Collage resulting images from TA section immunofluorescence against Laminin (green) and αSarcoglycan (αSG) (red) revealing morphology and overall αSG expression recovery areas (arrows in b) upon H2 intramuscular injection c, d comparing with A6 infusion a, b. b, d Enlarged view of dashed boxes showing still small, centre-nucleated degenerating myofibers (arrowheads) after A6 graft b and αSG expression (arrows) and recovered morphology - myofibers with uniform size—upon cell clone injection d nuclei were labeled by DAPI (blue). e Fibres Cross Sectional Analysis (CSA) highlights the muscle recovery due to H2 effect on αSGKO dystrophic muscle, presenting the disappearance of small (under 500 μm2) degenerating muscle fibres

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