Fig. 5: Misplaced LCO causes reduced coronary flow, leading to lethal anomalous coronary arteries.
From: A SOX17-PDGFB signaling axis regulates aortic root development
a Representative whole heart smMHC IF images (n = 5/group) of E16.5 control and Sox17eKO hearts show narrowed LCA (arrow) and collateral vessels extended from RCA to LCA (arrowheads) in the mutant hearts. b Representative images of whole heart PECAM1 IF (n = 3/group) of E16.5 control and Sox17eKO embryos show narrowed LCA (arrows) in Sox17eKO hearts. c, d Representative IF images (n=5/group) of E16.5 control and Sox17eKO hearts shows reduced endothelial expression of KLF4 (red, arrow) in LCO (c) and LCA (d) of Sox17eKO hearts. e Quantitative analysis of (c, d) confirms reduced aortic-coronary flow at LCO. (n = 5/group, mean ± SD, unpaired two-tailed t-test, p = 0.001 for LCO, p = 0.0014 for LCA, *p < 0.05). f Computational simulation shows reduced wall sheer stress (WSS) from 82 to 55 cgs (centimetre–gram–second system of units) at LCO in E16.5 Sox17eKO hearts. g, h Representative hypoxia probe staining images (n = 4/group) of E13.5 or E15.5 control and Sox17eKO hearts shows severe hypoxia developed in the left ventricle (LV) of E15.5 Sox17eKO hearts (h), which also affects the right ventricle (RV) after the establishment of coronary circulation around E14.5, but not E13.5 Sox17eKO hearts before functional coronary circulation starts (g). Source data are provided as a Source Data file. Scale bars: 500 µm in a, b, g, h; 50 µm in c, d.
