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. 2020 Apr 23;40(6):1559–1573. doi: 10.1161/ATVBAHA.120.314297

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© 2020 The Authors.

Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 2. — EP4 (prostaglandin E receptor 4) heterozygous knockout in vascular smooth muscle cells inhibited abdominal aortic aneurysm and rupture after Ang II (angiotensin II) infusion. A, Representative images of aorta for EP4^fl/+;ApoE^−/⁻ and EP4^fl/+;SM22-Cre;ApoE^−/⁻ mice before and after Ang II infusion. Scale bars=1 mm. B and D, Maximum aortic diameter and elastin degradation grade of the aorta in EP4^fl/+;ApoE^−/⁻ and EP4^fl/+;SM22-Cre;ApoE^−/⁻ mice infused with Ang II. n=9 to 13. C, Elastica van Gieson–stained sections of the abdominal aorta for EP4^fl/+;ApoE^−/⁻ and EP4^fl/+;SM22-Cre;ApoE^−/⁻ mice after Ang II infusion. Scale bars=500 μm. ApoE^−/− indicates apolipoprotein E knockout; and NS, not significant. *P<0.05, **P<0.01, ***P<0.001.