Figure 3.

ABRO1 OE inhibits cardiomyocyte proliferation and cardiac regeneration in neonatal hearts

(A–D) AAV9 vector carrying Abro1 (ABRO1 OE) or negative control (Con OE) were administered to adult WT mice. The left ventricular FS% (A) and heart to body weight ratio (B) were measured at 21 days after AAV9 administration (n = 6–8 mice per group). (C) Representative images of hematoxylin-eosin-stained transverse sections of hearts at 21 days post AAV9 administration (scale bar, 2 mm). (D) Wheat germ agglutinin (WGA) staining of ventricular sections (scale bar, 20 μm) (left) and cardiomyocyte surface area (right) was measured at 21 days post AAV9 administration (n = 8 mice per group). (E) Adenovirus harboring Abro1 (ABRO1 OE) or negative control (Con OE) were administered to WT mice (at P1) and samples were collected at day 7 (P7). Representative confocal images of heart sections co-stained with pH3 (red), cTNT (green), and the nucleus (DAPI, blue) (scale bar, 25 μm) (left), and pH3-positive (right) cardiomyocytes were calculated (n = 8 mice per group). (F–I) The neonatal mice (P1) were administered with adenoviral ABRO1 (ABRO1 OE) or negative control (Con OE) and subjected to MI. (F) Quantification of the number of pH3-positive cardiomyocytes in heart sections at 7 days after MI (n = 8 mice per group). (G) Representative images of Masson’s trichrome-stained cross sections of hearts (scale bar, 2 mm). (H) The infarct size was quantified using length-based measurements at P7 post MI (n = 7 mice per group). (I) Echocardiography analysis of FS (n = 7 mice per group) at P7 post MI. All data are mean ± SD.