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. 2021 Mar 9;4(5):e202000997. doi: 10.26508/lsa.202000997

Figure 2. Carotid arteries from 2-mo WT and Hutchinson–Gilford Progeria Syndrome (HGPS) mice display similar histology.

Figure 2.

(A, B) Carotid artery cross sections from 2-mo WT and Hutchinson–Gilford Progeria Syndrome mice were stained with H&E (scale bar = 50 μm and inset bar = 25 μm), and the number of medial smooth muscle cell nuclei was quantified from H&E images (n = 7–10 carotids per genotype with three sections analyzed per mouse). (C, D) Carotid cross sections were immunostained for the senescence marker, p16INK4A, and the level of medial p16INK4A was normalized to the mean signal intensity of carotid sections from 2-mo WT mice; (n = 6–10 per genotype). Scale bar = 50 μm. Statistical significance in (B) and (D) was determined by Mann–Whitney tests. (E, F) Carotid cross sections were stained with Alizarin Red (n = 5 per genotype) and (F) immunostained for cleaved caspase-3 (n = 5 per genotype). Scale bars in (E) and (F) = 50 μm. The arterial media (M) is outlined with dashed lines.