Extended Data Fig. 9: Infusion of Ang II predisposed SMC-Aldh18a1−/− mice to lethal aortic dissection and rupture. | Nature Cardiovascular Research

Extended Data Fig. 9: Infusion of Ang II predisposed SMC-Aldh18a1−/− mice to lethal aortic dissection and rupture.

From: Mitochondrial NAD+ deficiency in vascular smooth muscle impairs collagen III turnover to trigger thoracic and abdominal aortic aneurysm

Extended Data Fig. 9

a, Representative immunohistologic images showing the staining of type I and III collagens in mice aortas in 3-day Ang II infused mouse model (n = 3 biological replicates). Scale bar: 50 μm. b, The Experimental outline of 6-weeks Ang II infusion. Osmotic minipumps were implanted subcutaneously in SMC-Aldh18a1−/− mice male mice for continuous delivery of Ang II over a period of 6 weeks. c, Incidence and localization of lethal aortic dissections. Within 6 weeks of Ang II treatment, SMC-Aldh18a1−/− mice exhibits a mortality rate of 5/10. d, Representative macroscopic images of the whole aortas of mice that died from aortic rupture (second line) and euthanized mice at the end of experiment (first line) in each group. Postmortem examination reveals that all deceased mice exhibited aortic ruptures with accompanying hemothorax or hemoabdomen, while the surviving mice demonstrate aortic dilation and intramural hematoma. Scale bar: 1 cm. e, Representative histologic images showing HE and EVG staining of ascending thoracic aorta and abdominal aorta of surviving mice euthanized at the end of experiment (n = 3 biological replicates). Histological assessment of the aorta indicates hematomas, elastin lamina degradation, and medial thickening in the aortas of surviving mice. Scale bar: 100 μm and 50 μm.

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