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. 2017 Jan 31;7:41756. doi: 10.1038/srep41756

Figure 6. Homed BM Sca-1+ cells stimulated cell proliferation through activation of PDGFRβ -Akt/p27 Kip1 signaling.

Figure 6

Phosphorylation of Erk1/2 and total Erk1/2 in the infarcted myocardium of Sca-1+ [(YSca1+)-O] and Sca-1− [(YSca1−)-O] chimeras 3 days post-myocardial infarction (MI) is depicted with GAPDH used as a control (A, n = 3–7/group). Phosphorylation of Akt and total Akt in the infarcted myocardium 3 days post-MI [LAD3] (B, n = 3–7/group) with GAPDH used as a control. The level of p27Kip1 determined by Western blot and normalized by GAPDH in the infarcted myocardium 3 days post-MI (C, n = 3/group). Quantification of cells entering S/G2 phase by propidium iodide (PI) staining in the infarcted chimeric hearts 3 days post-MI (D, n = 3/group). GAPDH: glyceraldehyde 3-phosphate dehydrogenase; LAD: ligation of left anterior coronary artery. Data analysis used two-way ANOVA followed by Bonferroni post-hoc tests for multiple comparisons (A,B,C,D). Data shown are mean ± SEM.