nox1 and nox2 knockdown or treatment with ROS and NADPH oxidase inhibitors rescues the cardiac phenotype by decreasing ROS levels. Lateral views of Tg(cmlc2::mCherry‐Ras)sd21 embryos stained with DCFH‐DA (5 μM) at 48 hpf following morpholino knockdown of hace1 (A), injection of control morpholino (B), morpholino knockdown of nox1 (C), nox2 (D), nox1/nox2 (E), and knockdown combination of hace1/nox1/nox2 (F). Co‐injection of hace1 MO + nox1/nox2 MOs rescues the abnormal cardiac phenotypes demonstrating the lowest levels of ROS and normal cardiac structure (F). Quantification of abnormal cardiac phenotypes in hace1 morphants following treatment with (G) NAC, ** P < 0.0001, and (H) Apo, ** P = 0.0098. The number on top of each bar represents the total number of embryos in the group. Scale bar = 250 µm. DCFH‐DA = 2',7'‐dichlorofluorescein diacetate.
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