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. Author manuscript; available in PMC: 2013 Nov 5.
Published in final edited form as: Ann Thorac Surg. 2013 Jul;96(1):10.1016/j.athoracsur.2013.04.005. doi: 10.1016/j.athoracsur.2013.04.005

Fig 4.

Fig 4

Early fetal cardiac cell proliferation is not affected by stromal-derived factor-1α (SDF1a) inhibition (SDFi). (A) Representative immunohistochemistry for 5-bromo-2-deoxyuridine (BrdU; red) and nkx2.5 (green) 3 days after myocardial infarction (MI). Representative images of the borderzone region of sham (top row), untreated (middle row), and mutant SDF-1α transgene SDFi-treated (bottom row) fetal infarcts are shown. (B) Comparable populations of proliferating cardiac progenitor cells (BrdU+ and nkx2.5+) were observed in the apex and remote regions. Mean population of cardiac progenitor cells in the borderzone in untreated fetal hearts increased by 24.8 cells/high-powered field (hpf; *p < 0.001) and 15.7cells/hpf in SDFi treated hearts (**p < 0.001). Error bars correspond to the 95% confidence interval.