Fig. 1

Alpha 1-adrenergic receptor signaling is a key regulator of cardiomyocyte and macrophage response to cardiac injury (A) 7 dpf myl7:H2B-GFP; csf1ra:Gal4; UAS:NTR-mCherry larvae in which the cardiac ventricles were injured focally with a two-photon laser, and uninjured siblings, after 24 h application of carvedilol, propranolol, prazosin, atropine, or control solution. 16 h EdU pulse-labeled cells undergoing DNA synthesis are in magenta. Cardiomyocytes and macrophages were immunostained with GFP and mCherry, respectively. EdU and GFP channels of the composite images are shown here. Dashed lines outline injury areas. White circles mark proliferating cardiomyocytes. (B–E) Bar graphs depicting percentages of EdU+ cardiomyocytes in the cardiac ventricles of carvedilol-treated (B), propranolol-treated (C), prazosin-treated (D), and atropine-treated (E) groups. (F) Uninjured and two-photon-injured cardiac ventricles of 7 dpf myl7:H2B-GFP; csf1ra:Gal4; UAS:NTR-mCherry larvae from the same experiment as in (A)–(E) showing GFP and mCherry channels of the composite images. Dashed lines outline injury areas. (G–J) Bar graphs depicting numbers of macrophages recruited to the ventricle of carvedilol-treated (G), propranolol-treated (H), prazosin-treated (I), and atropine-treated (J) groups. All scale bars: 20 μm. Data are presented as mean ± SEM, with data points of individual animals. n denotes number of animals used for each group. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; n.s., not significant; two-tailed t test.