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. 2017 Jan 24;6(1):e004968. doi: 10.1161/JAHA.116.004968

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© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Aortopathy in young MFS mice is worsened by loss of SMC TBRII. A through C, Representative sections of ascending aortas of 8‐week‐old mice, 2 weeks after treatment with tamoxifen. Sections are from (A) an Acta2‐Cre^0/0 Fbn1 ^+/+ mouse (WT), (B) an Acta2‐Cre^0/0 Fbn1 ^C1039G/+ mouse [MFS(T)]; or (C) an Acta2‐Cre^+/0 Fbn1 ^C1039G/+ mouse (MFS‐TBRII ^−/−). All mice were Tgfbr2 ^flox/flox. A through C, Scale bar: 100 μm. D and E, Measurements made on sections of ascending aorta of groups in A through C. D, Length of internal elastic lamina (IEL); (E) length of external elastic lamina (EEL); (F) medial elastin damage was quantified by counting elastin breaks on sections of ascending aorta of groups in A through C. G, Aortic medial degeneration was graded with an aortic wall architecture score. D through G, Data are mean±SEM; n=7 to 8 per group; t tests with Bonferroni correction; *P<0.05; ***P<0.001. MFS indicates Marfan syndrome; SMC, smooth muscle cells; (T), tamoxifen; TBRII, type II TGF‐β receptor; WT, wild‐type.