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. 2020 Sep 10;9:e60683. doi: 10.7554/eLife.60683

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© 2020, Nandadasa et al

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Figure 5. — (a) Aggrecan (green) and α-SMA staining (red) in E18.5 umbilical cords show loss of aggrecan and weak α-SMA staining in Acan^-/- vessels (n = 3 umbilical cords each genotype). (b) Smooth muscle myosin heavy chain (SMMHC, red) and phosphorylated myosin light chain (pMLC, green) staining in E18.5 umbilical cords showing dramatic signal attenuation in the Acan^-/- vessels (n = 3 umbilical cords each genotype) (c) pMLC (green), endomucin (red), α-SMA (red, center panels) and SMMHC (red, right-hand panels) staining shows blunted dimorphism of Adamts1^-/- umbilical artery and vein with stronger expression of differentiated SMC markers in Adamts1^-/- umbilical vessels and acquisition of endomucin, a venous endothelium marker, by arterial endothelium (n = 3 umbilical cords each genotype) Scale bars = 100 μm in (a–c).