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. 2015 Dec 1;142(23):4026–4037. doi: 10.1242/dev.126649

Fig. 2.

Fig. 2.

Depletion of miR-101a expression promotes cardiomyocyte proliferation in the injured apex. (A-D) Control or Tg(hs:miR-101a-sp) animals were injured and subjected to daily heat treatment. Hearts were collected at 3 dpa for histology, cryosectioned at 10 µm and stained with antibodies to detect Mef2 (green) and Pcna (red) to identify proliferating cardiomyocytes (CMs) (arrowheads) at the injured apex (A,C) and lateral wall (remote zone) (B,D). Insets in A,C are higher magnifications of the areas within dashed boxes. (E) CM proliferation indices were determined by representing Mef+Pcna+ cells as a percentage of total Mef2+ cells. Depletion of miR-101a expression doubled CM proliferation indices at 3 dpa in the injured apex but not in the remote zone. (F) qPCR studies show ∼80% reduction of miR-101a expression levels in Tg(hs:miR-101a-sp) ventricles  (blue line) compared with the control group (red dashed line) under conditions of heat treatment. n=5-7; *P<0.05 (Student's t-test); error bars represent s.e.m. HT, heat treatment.