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. Author manuscript; available in PMC: 2020 Dec 1.
Published in final edited form as: J Mol Cell Cardiol. 2019 Oct 19;137:82–92. doi: 10.1016/j.yjmcc.2019.10.003

Figure 3. Deletion of Sam68 in the BM accelerates re-endothelialization and attenuates neointima hyperplasia.

Figure 3.

BMT was performed using Sam68−/− or WT BM to reconstitute WT mice and 1 month later, wire-induced carotid injury was performed in the recipients that demonstrated a BM engraftment >85%. (A-B) At day 5 post-injury, mice were perfused with Evan’s blue and euthanized. (A) Representative Evans blue-stained arteries (bar=1 mm). (B) Quantification of re-endothelialized areas (n=5 per group). (C-D) Representative cross-section H.E. staining (C, scale bar=100μm) and quantification of neointima areas (D, n=5 per group) of carotid arteries isolated at day 28 post-injury. (E-F) Immunofluorescence staining of CD68 (E, green staining, white arrows) and quantification of CD68+ macrophages (F) in the injured vessels isolated at day 5 post-injury (n=5 per group). A two-tailed Student’s t-test was used in B, D, and F for statistical analysis. Error bars represent mean ± SEM.