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. Author manuscript; available in PMC: 2021 May 28.
Published in final edited form as: Cell Rep. 2021 May 4;35(5):109088. doi: 10.1016/j.celrep.2021.109088

Figure 6. Sarcomere-deficient CMs enhance in vivo cardiac engraftment.

Figure 6.

(A) Overview of experimental workflow used to study cardiac engraftment of human CMs in a rat model of myocardial infarction (MI).

(B) Representative immunohistochemistry images and (C) quantification of rat left ventricle (LV) sections stained for human β-myosin heavy chain (β-MHC) to assess human CM graft size, which was increased when using TnI-DKO CMs compared to WT. Scale bar, 250 μm.

(D–G) Representative immunofluorescence images and quantification of rat LV sections probed for β-MHC (green; human CMs), Hoechst (blue; nuclei), and either (D and E) BrdU (magenta; cumulative proliferation) or (F and G) Ki67 (magenta; active proliferation), which show increased % BrdU+ and %Ki67+ human CMs when using TnI-DKO for engraftment, demonstrating enhanced proliferative capacity compared to WT CMs. Scale bars, 25 μm (D) or 50 μm (F).

Data are n ≥ 3 and mean ± SEM; significance assessed by t test and defined by *p ≤ 0.05 and **p ≤ 0.01. See also Figure S6.