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Fig. 5
Long-term miR-101a depletion results in muscle regeneration and defects in scar tissue clearance. (A-F) Control, Tg(hs:miR-101a-sp) and Tg(hs:miR-133a1-pre) hearts were resectioned, heat treated daily for 30dpa and extracted for histology. Hearts were cryosectioned at 10µm and stained with either AFOG (A-C) or antibodies directed against Tropomyosin (D-F). Compared with heat-treated control animals, Tg(hs:miR-101a-sp) hearts reveal more scar tissue and less new muscle regeneration in the wounded apex. Tg(hs:miR-133a1-pre) hearts, which overexpress miR-133a1, show defects in both new muscle regeneration and scar tissue removal. Brackets represent approximate injury area; arrowheads in F mark gaps in myocardium and the lack of muscle regeneration. (G-I) Quantification of scarring indices, Tropomyosin expression and injury area were performed with CellProfiler. n=6-7; *P<0.05 (Student′s t-test); error bars represent s.e.m.